The present invention is related to a chemical compound; an inhibitor of fibroblast activation protein (FAP); a composition comprising the compound and inhibitor, respectively; the compound, the inhibitor and the composition, respectively, for use in a method for the diagnosis of a disease; the compound, the inhibitor and the composition, respectively, for use in a method for the treatment of a disease; the compound, the inhibitor and the composition, respectively, for use in a method of diagnosis and treatment of a disease which is also referred to as "thera(g)nosis" or "thera(g)nostics"; the compound, the inhibitor and the composition, respectively, for use in a method for delivering an effector to a FAP-expressing tissue; a method for the diagnosis of a disease using the compound, the inhibitor and the composition, respectively; a method for the treatment of a disease using the compound, the inhibitor and the composition, respectively; a method for the diagnosis and treatment of a disease which is also referred to as "thera(g)nosis" or "thera(g)nostics, using the compound, the inhibitor and the composition, respectively; a method for the delivery of an effector to a FAP-expressing tissue using the compound, the inhibitor and the composition, respectively.

Despite the increasing availability of therapeutic options, cancer is still the second leading cause of death globally. Therapeutic strategies mainly focus on targeting malignant cancer cells itself, ignoring the ever-present surrounding tumor microenvironment (TME) that limit the access of therapeutic cancer cell agents (Valkenburg, et al., Nat Rev Clin Oncol, 2018, 15: 366). The TME is part of the tumor mass and consists not only of the heterogeneous population of cancer cells but also of a variety of resident and infiltrating host cells, secreted factors, and extracellular matrix proteins (Quail, et al., Nat Med, 2013, 19: 1423). A dominant cell type found in the TME is the cancer associated fibroblast (CAF) (Kalluri, Nat Rev Cancer, 2016, 16: 582). Many different cell types have been described as the source and origin for CAFs, such as e.g. fibroblasts, mesenchymal stem cells, smooth muscle cells, cells of epithelial origin, or endothelial cells (Madar, et al., Trends Mol Med, 2013, 19: 447). CAFs exhibit mesenchymal-like features and often are the dominant cell type within a solid tumor mass. CAFs have attracted increasing attention as a player in tumor progression and homeostasis (Gascard, et al., Genes Dev, 2016, 30: 1002; LeBleu, et al., Dis Model Mech, 2018, 11).

During recent years, fibroblast activation protein (FAP) has gained notoriety as a marker of CAFs (Shiga, et al., Cancers (Basel), 2015, 7: 2443; Pure, et al., Oncogene, 2018, 37: 4343; Jacob, et al., Curr Mol Med, 2012, 12: 1220). Due to the omnipresence of CAFs and stroma within tumors, FAP was discovered as a suitable marker for radiopharmaceutical diagnostics and as a suitable target for radiopharmaceutical therapy (Siveke, J Nucl Med, 2018, 59: 1412).

Fibroblast activation protein α (FAP) is a type II transmembrane serine protease and a member of the S9 prolyl oligopeptidase family (Park, et al., J Biol Chem, 1999, 274: 36505). The closest family member DPP4 shares 53% homology with FAP. Like other DPP enzymes (DPP4, DPP7, DPP8, DPP9), FAP has post-proline exopeptidase activity. In addition, FAP possesses endopeptidase activity, similar to prolyl oligopeptidase/endopeptidase (POP/PREP). The FAP gene is highly conserved across various species. The extracellular domain of human FAP shares 90% amino acid sequence identity with mouse and rat FAP. Mouse FAP has 97% sequence identity with rat FAP.

Structurally, FAP is a 760 amino acid transmembrane protein composed of a short N-terminal cytoplasmic tail (6 amino acids), a single transmembrane domain (20 amino acids), and a 734 amino acid extracellular domain (Aertgeerts, et al., J Biol Chem, 2005, 280: 19441). This extracellular domain consists of an eight-bladed β-propeller and an α/β hydrolase domain. The catalytic triad is composed of Ser624, Asp702, and His734 and is located at the interface of the β-propeller and the hydrolase domain. The active site is accessible through a central hole of the β-propeller domain or through a narrow cavity between the β-propeller and the hydrolase domain. FAP monomers are not active, but form active homodimers as well as heterodimers with DPP4 (Ghersi, et al., Cancer Res, 2006, 66: 4652). Soluble homodimeric FAP has also been described (Keane, et al., FEBS Open Bio, 2013, 4: 43; Lee, et al., Blood, 2006, 107: 1397).

FAP possesses dual enzyme activity (Hamson, et al., Proteomics Clin Appl, 2014, 8: 454). Its dipeptidyl peptidase activity allows cleaving two amino acids of the N-terminus after a proline residue. FAP substrates that are cleaved rapidly via its dipeptidyl peptidase activity are neuropeptide Y, Peptide YY, Substance P, and β-type natriuretic peptide. Collagen I and III, FGF21 and α₂-antiplasmin have been shown to be cleaved by the endopeptidase activity of FAP. While FAP is unable to cleave native collagens, pre-digestion by other proteases, such as matrix metalloproteinases, facilitates further collagen cleavage by FAP. Processing of collagen may influence migratory capacities of cancer cells. Besides increasing invasiveness of cancer cells through remodeling of the extracellular matrix, several other FAP-mediated tumor promoting roles have been proposed, including proliferation and increasing angiogenesis. Furthermore, stromal expression of FAP is linked to escape from immunosurveillance in various cancers, suggesting a role in anti-tumor immunity (Pure, et al., Oncogene, 2018, 37: 4343).

FAP is transiently expressed during normal development, but only rarely in healthy adult tissues. In transgenic mice, it was demonstrated that FAP is expressed by adipose tissue, skeletal muscle, skin, bone and pancreas (Pure, et al., Oncogene, 2018, 37: 4343; Roberts, et al., J Exp Med, 2013, 210: 1137). However, a FAP knockout mouse has a healthy phenotype, suggesting a redundant role under normal conditions (Niedermeyer, et al., Mol Cell Biol, 2000, 20: 1089). At sites of active tissue remodeling, including wound healing, fibrosis, arthritis, atherosclerosis and cancer, FAP becomes highly upregulated in stromal cells (Pure, et al., Oncogene, 2018, 37: 4343).

FAP expression in the tumor stroma of 90% of epithelial carcinomas was first reported in 1990 under use of a monoclonal antibody, F19 (Garin-Chesa, et al., Proc Natl Acad Sci USA, 1990, 87: 7235; Rettig, et al., Cancer Res, 1993, 53: 3327). FAP-expressing stromal cells were further characterized as cancer-associated fibroblasts (CAF) and cancer-associated pericytes (Cremasco, et al., Cancer Immunol Res, 2018, 6: 1472). FAP expression on malignant epithelial cells has also been reported but its significance remains to be defined (Pure, et al., Oncogene, 2018, 37: 4343). The following Table 1, taken from Busek et al. (Busek, et al., Front Biosci (Landmark Ed), 2018, 23: 1933), summarizes the expression of FAP in various malignancies indicating the tumor type and the cellular expression. Tumor Type Expression of FAP in Malignant Cells Expression of FAP in Stroma Cells Notes Basal cell carcinoma, squamous cell carcinoma of the skin - + Expression in fibroblasts strongest in close proximity to cancer cells. FAP expression is absent in benign epithelial tumors, its positivity in the stroma may be a useful criterion for differentiating between morpheaform/infiltrative basal cell carcinomas and FAP-negative desmoplastic trichoepithelioma. Oral squamous cell carcinoma + + FAP is a negative prognostic marker_elevated expression is associated with greater tumor size, lymph-node metastasis, advanced clinical stage, and worse overall survival. Melanoma - (in situ) + FAP expression present in a subset of melanocytes in 30% of benign melanocytic nevi, but not detectable in malignant melanoma cells in melanoma tissues. The quantity of FAP-positive stromal cells is positively associated with ECM content and inflammatory cell infiltration. Normal melanocytes express FAP in vitro Conflicting data for FAP in melanoma cells: several human melanoma cell lines express FAP and FAP contributes to their invasiveness in vitro, but immunopositivity has not been detected in melanoma tissues. Mouse melanoma cell lines are FAP-negative and mouse FAP is a tumor suppressor independently of its enzymatic activity. Esophageal cancer + + FAP is expressed in cancer cells as well as in premalignant metaplastic cells of the esophagus in both adenocarcinoma and squamous cell carcinoma. Gastric cancer + + (incl. low expression in endothelial cells) A higher stromal FAP expression at the invasion front is associated with low tumor cell differentiation, more advanced TNM stage, serosal invasion, and poor survival. A higher stromal FAP is associated with worse survival. A higher FAP expression in intestinal-type gastric cancer (in stroma, moderately differentiated cancer cells, and endothelial cells) than in the diffuse type (mainly in cancer cells with poor cell-to-cell contacts, endothelial cells). A higher stromal FAP expression in the intestinal-type gastric cancer is associated with the presence of liver and lymph node metastases. Colorectal cancer + + A higher stromal FAP positivity found in earlier-stage disease, but in patients with stage IV tumors high FAP is associated with worse survival. A higher FAP expression is associated with advanced Duke stage. A high FAP expression in the tumor center is a negative prognostic factor. Stromal FAP expression in stage II/III rectal cancer after chemoradiotherapy is associated with a worse prognosis. A higher FAP mRNA expression is associated with worse disease-free survival and a trend for worse overall survival. Pancreatic adenocarcinoma + + FAP expression in carcinoma cells is associated with a larger tumor size, presence of a fibrotic focus, perineural invasion, and a worse prognosis. Stromal FAP expression correlates with lymph node metastasis and reduced survival. Nevertheless, a recent retrospective Korean study reports an association between a lower number of FAP+ fibroblasts and a decreased overall survival based on a univariate analysis. Hepatocellular carcinoma + FAP expression detected especially in tumors with abundant fibrous stroma. FAP mRNA expression increased in peritumoral tissue, positively correlating with the density of peritumoral activated HSCs. Higher levels are associated with more frequent early recurrence, larger tumor size, presence of vascular invasion, and an advanced TNM stage. Non-small cell lung cancer -/+ + Absence of stromal FAP expression (24% of cases) in NSCLC is associated with better survival. Reports regarding expression in cancer cells are inconsistent. Mesothelioma + + Expression, although to a variable extent, has been detected in all subtypes. Breast tumors + (ductal adenocarci noma) + (incl. endothelial cells FAP positivity detected mainly in the stroma; another study proposes a predominant localization in cancer cells in ductal adenocarcinoma. Jung et al. observed expression in cancer and stromal cells in 50% of cases where stroma is rich in adipose tissue (approximately 1/3 of all tumors); in these cases, FAP expression was associated with a higher tumor grade. In tumors with fibrous stroma, FAP expression was virtually absent (2/3 of all tumors) FAP expression is higher in cancer cells in lobular cancer than in ductal carcinoma. Stromal FAP and calponin positivity may be an ancillary marker for detecting microinvasion in ductal carcinoma. FAP expression increases with the malignant progression of phyllodes tumors, but a later study detected stromal FAP expression only in 12.5% of the malignant phyllodes tumors by IHC. Conflicting data regarding a possible association with breast cancer survival: smaller studies have reported that a higher total FAP mRNA expression is associated with worse survival, while a higher stromal FAP expression detected by IHC was associated with a longer overall survival and disease-free survival. A recent larger study involving 939 breast cancer patients did not prove any association between FAP expression in the cancer or stromal cells and survival. Renal cancer - + Stromal FAP expression (detected in 23% of cases) associated with markers of aggressiveness and worse survival in clear cell renal cell carcinoma. In metastatic clear cell renal carcinoma, stromal FAP expression was detected in 36% of primary and 44% of metastatic lesions, and was associated with several parameters of tumor aggressiveness and worse survival. Prostate cancer - + Only small patient cohorts reported in literature. Expression in stromal cells detected in 7/7 cases, most intense in stromal cells adjacent to cancer cells. Cervical cancer + + No FAP expression was detected in preinvasive cervical neoplasia (CIN1, 2), occasional positivity in stroma in CIN3 with moderate or severe inflammatory infiltrates. Enhanced expression of FAP was found in cancer cells and subepithelial stromal cells in some of the microinvasive and all of the invasive carcinomas. Ovary + + FAP positivity increases with tumor stage; negative FAP expression is associated with longer disease-free survival. FAP positivity detected in cancer cells in 21% of tumors, stromal positivity in 61%. Another study reported stromal positivity in 92% of cancer tissues with extremely rare FAP expression in malignant cells; it also reported an association with advanced tumor stage and presence of lymph node metastases. FAP-positive malignant cells are present in malignant pleural and peritoneal effusions: strong positivity is associated with worse survival. Glioma + + FAP expression increased in glioblastoma, highest expression found in the mesenchymal subtype and gliosarcoma. Low expression in glioma stem-like cells. In glioblastoma, overall FAP quantity is not associated with survival. Thyroid cancer - + FAP upregulated in aggressive papillary thyroid carcinomas. In medullary thyroid carcinoma, FAP expression in the peritumoral and intratumoral stromal compartment correlates with the degree of desmoplasia and presence of lymph node metastases. Parathyroid tumors n.d. + FAP mRNA expression was significantly higher in parathyroid carcinomas than in adenomas. Sarcomas + (see note) + (reactive fibroblasts in Ewing's sarcomas ) FAP expression found in malignant cells in fibrosarcomas, leiomyosarcoma, malignant fibrous histiocytoma, low grade myofibroblastic sarcoma, fibroblastic areas in osteosarcomas, osteoid osteoma, and in osteosarcoma. FAP is negative in malignant cells with "small round cell" phenotype (embryonal rhabdomyosarcoma, Ewing sarcoma, or mesenchymal chondrosarcoma). A higher expression in osteosarcoma associated with more advanced clinical stage, presence of distant metastasis, high histological grade, and a worse progression-free and overall survival. FAP is expressed in both malignant and benign tumors and its positivity reflects their histogenetic origin rather than malignant potential. Myeloma - + FAP expression was detected in osteoclasts, endothelial cells, adipocytes, fibrotic stroma, but not in multiple myeloma cells. FAP is upregulated in osteoclasts co-cultured with myeloma cells.

FAP expression in CAFs was shown for almost all carcinomas and sarcomas (Pure, et al., Oncogene, 2018, 37: 4343; Busek, et al., Front Biosci (Landmark Ed), 2018, 23: 1933). Furthermore, CAFs are present in hematological malignancies (Raffaghello, et al., Oncotarget, 2015, 6: 2589). Utilization of FAP as a therapeutic target is therefore not limited to certain tumor entities.

The abundance of FAP-expressing CAFs is described to correlate with poor prognosis. Across a wide range of human tumor indications, FAP expression is described to correlate with higher tumor grade and worse overall survival (Pure, et al., Oncogene, 2018, 37: 4343).

As described above, it is indicated that FAP as well as FAP-expressing cells present in the tumor microenvironment significantly influence tumor progression (Hanahan, et al., Cancer Cell, 2012, 21: 309). Additionally, due to its relatively selective expression in tumors, FAP is regarded as a suitable target for therapeutic and diagnostic agents as described below (Siveke, J Nucl Med, 2018, 59: 1412; Christiansen, et al., Neoplasia, 2013, 15: 348; Zi, et al., Mol Med Rep, 2015, 11: 3203).

Soon after its discovery, FAP was utilized as a therapeutic target in cancer. Until today, various strategies have been explored, including e.g. inhibition of FAP enzymatic activity, ablation of FAP-positive cells, or targeted delivery of cytotoxic compounds.

In 2007, an inhibitor of FAP and DPP4, Talabostat (Val-boro-Pro, PT-100), was developed by Point Therapeutics (for example as described in U.S. patent No. 6,890,904, WO9916864). Pennisi et al. (Pennisi, et al., Br J Haematol, 2009, 145: 775) observed a reduced tumor growth in a multiple myeloma animal model as well as in cancer syngeneic mouse models. Furthermore, several other prolyl boronic acid derivatives have been developed and reported as putative selective inhibitors for FAP. These derivatives show instability in aqueous environments at physiologic pH (Coutts, et al., J Med Chem, 1996, 39: 2087) and a non-specific reactivity with other enzymes.

WO 2008/116054 disclosed hexapeptide derivatives wherein compounds comprise a C-terminal bis-amino or boronic acid functional group.

US 2017/0066800 disclosed pseudopeptide inhibitors, such as M83, effective against FAP. These inhibitors were assessed in lung and colon cancer xenografts in immunodeficient mice. A suppression of tumor growth was observed (Jackson, et al., Neoplasia, 2015, 17: 43). These pseudopeptides inhibit the activity of both prolyl oligopeptidase (POP/PREP) and FAP, thereby excluding their use as specific therapeutic FAP inhibitors.

US 2008/280856 disclosed a nanomolar boronic acid-based inhibitor. The inhibitor shows a bispecific inhibition of FAP and PREP, thereby excluding their use as specific therapeutic FAP inhibitors.

FAP inhibitors based on cyclic peptides were disclosed, e.g., in WO 2016/146174 and WO 2006/042282. WO 2016/146174 disclosed peptides for diagnosis and treatment of tumors expressing FAP showing specificity for FAP, whereby closely related homologue DPP4 was not recognized by said peptides. WO 2006/042282 disclosed polypeptides for treatment of melanoma. In nude mice, inhibition of melanoma growth and melanoma metastasis was shown.

WO 99/75151 and WO 01/68708 disclosed a humanized FAP monoclonal antibody, F19, (Sibrotuzumab). Furthermore, the anti-FAP antibody F19 and humanized versions thereof were disclosed in WO 99/57151 and WO 01/68708. Development approaches involved e.g. the generation of high affinity, species cross-reactive, FAP-specific scFvs converted into a bivalent derivative (Brocks, et al., Mol Med, 2001, 7: 461). In Phase I and II clinical trials, Sibrotuzumab showed specific tumor enrichment whilst failing to demonstrate measurable therapeutic activity in patients with metastatic colorectal cancer, with only 2 out of 17 patients having stable disease (Hofheinz, et al., Onkologie, 2003, 26: 44). This F19 antibody has not been shown to block any cellular or protease function of FAP, which might explain the lack of therapeutic effects (Hofheinz, et al., Onkologie, 2003, 26: 44; Scott, et al., Clin Cancer Res, 2003, 9: 1639).

US 2018/022822 disclosed novel molecules specifically binding to human FAP and epitopes thereof, as human-derived antibodies and chimeric antigen receptors (CARs) useful in the treatment of diseases and conditions induced by FAP. Treatment of mice bearing orthotopic syngeneic MC38 colorectal tumors with an anti-FAP antibody reduced the tumor diameter and number of metastasis. WO 2012/020006 disclosed glycoengineered antibodies that bear modified oligosaccharides in the Fc region. Subsequently, bispecific antibodies specific for FAP and DR5 were developed as subject to WO 2014/161845. These antibodies trigger tumor cell apoptosis in vitro and in in vivo preclinical tumor models with FAP-positive stroma (Brunker, et al., Mol Cancer Ther, 2016, 15: 946). Antibody drug conjugates and immunotoxins that target FAP are described in WO 2015/118030. In vitro toxicity as well as in vivo inhibition of tumor growth was shown following application of anti-hu/moFAP hu36:cytolysin ADC candidates. It is unclear whether these antibodies were capable of inhibiting FAP activity.

Small molecule FAP inhibitors based on (4-quinolinoyl)glycyl-2-cyanopyrrolidine displaying low nanomolar inhibitory potency and high selectivity against related DPPs and PREP were described by Jansen et al. (Jansen, et al., J Med Chem, 2014, 57: 3053; Jansen, et al., ACS Med Chem Lett, 2013, 4: 491) and disclosed in WO 2013/107820. However, the compounds are structurally unrelated to the compounds of the present invention and include a war-head leading to covalent binding to FAP.

In recent years, several FAP-targeted radiopharmaceutical approaches were developed which are exemplarily described herein.

WO 2010/036814 disclosed small molecule inhibitors of FAP for use as therapeutic agents through inhibition of FAPs enzyme activity or as radiopharmaceuticals through binding to FAP.

WO 2019/083990 disclosed imaging and radiotherapeutic agents based on small molecule FAP-inhibitors described by Jansen et al. (Jansen, et al., J Med Chem, 2014, 57: 3053; Jansen, et al., ACS Med Chem Lett, 2013, 4: 491). Furthermore, several authors described selective uptake in tumors of cancer patients of imaging and radiotherapeutic agents (Lindner, et al., J Nucl Med, 2018, 59: 1415; Loktev, et al., J Nucl Med, 2018, 59: 1423; Giesel, et al., J Nucl Med, 2019, 60: 386; Loktev, et al., J Nucl Med, 2019, Mar 8 (epub ahead of print); Giesel, et al., Eur J Nucl Med Mol Imaging, 2019, 46: 1754; Kratochwil, et al., J Nucl Med, 2019, 60: 801) based on FAP-inhibitors described by Jansen et al. (Jansen, et al., J Med Chem, 2014, 57: 3053; Jansen, et al., ACS Med Chem Lett, 2013, 4: 491).

Clinical assessments of a ¹³¹I-labeled, humanized form of the F19 antibody (sibrotuzumab) revealed a selective uptake by tumors but not by normal tissues in patients with colorectal carcinoma or non-small cell lung cancer (Scott, et al., Clin Cancer Res, 2003, 9: 1639). This may be due to the long circulation time of antibodies that makes them unsuitable for a diagnostic, therapeutic, or theragnostic approach involving radionuclides.

WO 2011/040972 disclosed high-affinity antibodies recognizing both human and murine FAP antigen as potent radioimmunoconjugates. ESC11 lgG1 induces down modulation and internalization of surface FAP (Fischer, et al., Clin Cancer Res, 2012, 18: 6208). WO 2017/211809 disclosed tissue targeting thorium-227 complexes wherein the targeting moiety has specificity for FAP. However, the long circulation time of antibodies makes them unsuitable for a diagnostic, therapeutic, or theragnostic approach involving radionuclides.

FAP has also been described as being involved in other diseases than oncology indications, examples of which are given below.

Fibroblast-like synoviocytes in rheumatoid arthritic joints of patients show a significantly increased expression of FAP (Bauer, et al., Arthritis Res Ther, 2006, 8: R171; Milner, et al., Arthritis Res Ther, 2006, 8: R23). In rheumatoid arthritis, stromal cells play an important role in organizing the structure of synovial tissue of joints by producing extracellular matrix components, recruiting infiltrating immune cells and secreting inflammatory mediators. Considerable evidence exists supporting a role for these cells in driving the persistence of inflammation and joint damage (Bartok, et al., Immunol Rev, 2010, 233: 233; Turner, et al., Curr Opin Rheumatol, 2015, 27: 175). In rheumatoid arthritis FAP has a pathological role in cartilage turnover at least by promotion of proteoglycan loss and subsequently cartilage degradation (Bauer, et al., Arthritis Res Ther, 2006, 8: R171; Waldele, et al., Arthritis Res Ther, 2015, 17: 12). Therefore, it might serve as a marker for patient stratification, for evaluation and follow-up of treatment success, or as a therapeutic target (Bauer, et al., Arthritis Res Ther, 2006, 8: R171). In mice, a treatment response was demonstrated using SPECT/CT imaging of a ^99mTc-labeled anti-FAP antibody (van der Geest, et al., Rheumatology (Oxford), 2018, 57: 737; Laverman, et al., J Nucl Med, 2015, 56: 778; van der Geest, et al., J Nucl Med, 2017, 58: 151).

Additionally, FAP was recognized not only as a marker of activated fibroblasts in the injury response (Tillmanns, et al., Int J Cardiol, 2013, 168: 3926) but also as an important player in the healing process of wounds (Ramirez-Montagut, et al., Oncogene, 2004, 23: 5435). Jing et al. demonstrated a time-dependent course of change in FAP expression following burn wounds in rats (Jing, et al., Nan Fang Yi Ke Da Xue Xue Bao, 2013, 33: 615). Inhibiting of FAP activity in reactive wound fibroblasts in Keloid scars, common benign fibroproliferative reticular dermal lesions, might offer therapeutic option to prevent disease progression (Dienus, et al., Arch Dermatol Res, 2010, 302: 725).

In fibrotic diseases, upregulated expression of FAP was observed e.g. in idiopathic pulmonary fibrosis, Crohn's disease, and liver fibrosis. In an ex vivo model for Crohn's disease, a chronic bowel inflammatory disease characterized by an excessive, misbalanced extracellular matrix (ECM) deposition, upregulated FAP expression was observed. FAP inhibition reconstituted extracellular matrix homeostasis (Truffi, et al., Inflamm Bowel Dis, 2018, 24: 332). Similar observations were made by Egger et al. (Egger, et al., Eur J Pharmacol, 2017, 809: 64) under use of a murine model of pulmonary fibrosis. Inhibition of FAP leads to reduced fibrotic pathology. FAP is also expressed in the tissue remodelling region in chronically injured liver (Wang, et al., Front Biosci, 2008, 13: 3168), and FAP expression by hepatic stellate cells correlates with the histological severity of liver disease (Gorrell, et al., Adv Exp Med Biol, 2003, 524: 235). Therefore, FAP is also a promising target in the treatment of liver fibrosis (Lay, et al., Front Biosci (Landmark Ed), 2019, 24: 1).

FAP is expressed in arteriosclerotic lesions and upregulated in activated vascular smooth muscle cells (Monslow, et al., Circulation, 2013, 128: A17597). Monslow et al. showed that targeted inhibition of FAP in arteriosclerotic lesions may decrease overall lesion burden, inhibit inflammatory cell homing, and increase lesion stability through its ability to alter lesion architecture by favoring matrix-rich lesions over inflammation. More importantly, most of the arteriosclerotic pathologies share a common pathogenic feature: the rupture of an atherosclerotic plaque inducing arteriosclerotic lesions (Davies, et al., Br Heart J, 1985, 53: 363; Falk, Am J Cardiol, 1989, 63: 114e). Rupture of the fibrous cap in advanced atherosclerotic plaques is a critical trigger of acute coronary syndromes that may lead to myocardial infarction and sudden cardiac death. One of the key events in promoting plaque instability is the degradation of the fibrous cap, which exposes the underlying thrombogenic plaque core to the bloodstream, thereby causing thrombosis and subsequent vessel occlusion (Farb, et al., Circulation, 1996, 93: 1354; Virmani, et al., J Am Coll Cardiol, 2006, 47: C13). Brokopp et al. showed that FAP contributes to type I collagen breakdown in fibrous caps (Brokopp, et al., Eur Heart J, 2011, 32: 2713). A radiolabeled tracer was developed and its applicability for atherosclerosis imaging shown (Meletta, et al., Molecules, 2015, 20: 2081).

The problem underlying the present invention is the provision of a compound which is suitable as a diagnostic agent and/or a pharmaceutical agent, particularly if conjugated to a diagnostically and/or therapeutically active effector. A further problem underlying the present invention is the provision of a compound which is suitable as a diagnostic agent and/or a pharmaceutical agent, particularly if conjugated to a diagnostically and/or therapeutically active effector, whereby the compound is a potent inhibitor of FAP activity; preferably the pIC50 of the compound is equal to or greater than 6.0. A further problem underlying the present invention is the provision of a compound which is suitable as a diagnostic agent and/or a pharmaceutical agent, particularly if conjugated to a diagnostically and/or therapeutically active effector, in the diagnosis and/or therapy of a disease where the diseased cells and/or diseased tissues express FAP. A still further problem underlying the instant invention is the provision of a compound which is suitable for delivering a diagnostically and/or therapeutically effective agent to a diseased cell and/or diseased tissue, respectively, and more particularly a FAP-expressing diseased cell and/or diseased tissue, preferably the diseased tissue comprises or contains cancer associated fibroblasts. Also, a problem underlying the present invention is the provision of a method for the diagnosis of a disease, of a method for the treatment and/or prevention of a disease, and a method for the combined diagnosis and treatment of a disease; preferably such disease is a disease involving FAP-expressing cells and/or tissues, more particularly a FAP-expressing diseased cell and/or diseased tissue, preferably the diseased tissue comprises or contains cancer associated fibroblasts. A still further problem underlying the present invention is the provision of a method for the identification of a subject, wherein the subject is likely to respond or likely not to respond to a treatment of a disease, a method for the selection of a subject from a group of subjects, wherein the subject is likely to respond or likely not to respond to a treatment of a disease. Also, a problem underlying the present invention is the provision of a pharmaceutical composition containing a compound having the characteristics as outlined above. Furthermore, a problem underlying the present invention is the provision of a kit which is suitable for use in any of the above methods.

There is a need for compounds that are suitable as a diagnostic agent and/or pharmaceutical agent, particularly if conjugated to a diagnostically and/or therapeutically active effector. Furthermore, there is a need for compounds that are suitable as a diagnostic agent and/or a pharmaceutical agent, particularly if conjugated to a diagnostically and/or therapeutically active effector, whereby the compound is a potent inhibitor of FAP activity; preferably the pIC50 of the compound is equal to or greater than 6.0. Further, there is a need for compounds suitable as diagnostic agents and/or pharmaceutical agents, particularly if conjugated to a diagnostically and/or therapeutically active effector, in the diagnosis and/or therapy of a disease where the diseased cells and/or diseased tissues express FAP. Furthermore, there is a need for a compound which is suitable for delivering a diagnostically and/or therapeutically effective agent to a diseased cell and/or diseased tissue, respectively, and more particularly a FAP-expressing diseased cell and/or diseased tissue, preferably the diseased tissue comprises or contains cancer associated fibroblasts. Also, there is a need for a method for the diagnosis of a disease, of a method for the treatment and/or prevention of a disease, and a method for the combined diagnosis and treatment of a disease; preferably such disease is a disease involving FAP-expressing cells and/or tissues, more particularly a FAP-expressing diseased cell and/or diseased tissue, preferably the diseased tissue comprises or contains cancer associated fibroblasts. Furthermore, there is a need for a method for the identification of a subject, wherein the subject is likely to respond or likely not to respond to a treatment of a disease, a method for the selection of a subject from a group of subjects, wherein the subject is likely to respond or likely not to respond to a treatment of a disease. Further, there is a need for a pharmaceutical composition containing a compound having the characteristics as outlined above. Furthermore, there is a need for a kit which is suitable for use in any of the above methods. The present invention satisfies these needs.

These and other problems are solved by the subject matter of the attached claims.

These and other problems are also solved by the following embodiments. The invention is set out in the appended set of claims.

Embodiment 1. A compound selected from the group consisting of compound Hex-[Cys(tMeBn(DOTA-AET))-Pro-Pro-Thr-Gln-Phe-Cys]-OH (3BP-3554) of the following formula and compound Hex-[Cys(tMeBn(DOTA-PP))-Pro-Pro-Thr-Gln-Phe-Cys]-Asp-NH2 (3BP-3407) of the following formula

Embodiment 2. The compound of Embodiment 1, wherein the compound is compound Hex-[Cys(tMeBn(DOTA-AET))-Pro-Pro-Thr-Gln-Phe-Cys]-OH (3BP-3554) of the following formula

Embodiment 3. The compound of Embodiment 1, wherein the compound is compound Hex-[Cys(tMeBn(DOTA-PP))-Pro-Pro-Thr-Gln-Phe-Cys]-Asp-NH2 (3BP-3407) of the following formula

Embodiment 4. The compound of any one of Embodiments 1 to 3, wherein any S atom which can be oxidized, preferably S atoms of thioether groups, is present as -S-, -S(O)- or - S(O₂)- or a mixture thereof.

Embodiment 5. The compound of any one of Embodiments 1 to 4, wherein the compound is capable of binding to fibroblast activation protein (FAP).

Embodiment 6. The compound of any one of Embodiments 1 to 5, wherein the compound comprises a therapeutically active nuclide.

Embodiment 7. The compound of Embodiment 6, wherein the compound is selected from the group comprising compound Hex-[Cys(tMeBn(InDOTA-PP))-Pro-Pro-Thr-Gln-Phe-Cys]-Asp-NH2 (3BP-3590) of the following formula compound Hex-[Cys(tMeBn(LuDOTA-PP))-Pro-Pro-Thr-Gln-Phe-Cys]-Asp-NH2 (3BP-3591) of the following formula compound Hex-[Cys(tMeBn(GaDOTA-PP))-Pro-Pro-Thr-Gln-Phe-Cys]-Asp-NH2 (3BP-3592) of the following formula compound Hex-[Cys(tMeBn(EuDOTA-PP))-Pro-Pro-Thr-Gln-Phe-Cys]-Asp-NH2 (3BP-3661) of the following formula compound Hex-[Cys(tMeBn(InDOTA-AET))-Pro-Pro-Thr-Gln-Phe-Cys]-OH (3BP-3623) of the following formula compound Hex-[Cys(tMeBn(LuDOTA-AET))-Pro-Pro-Thr-Gln-Phe-Cys]-OH (3BP-3624) of the following formula compound Hex-[Cys(tMeBn(EuDOTA-AET))-Pro-Pro-Thr-Gln-Phe-Cys]-OH (3BP-3662) of the following formula compound Hex-[Cys(tMeBn(GaDOTA-AET))-Pro-Pro-Thr-Gln-Phe-Cys]-OH (3BP-3949) of the following formula compound Hex-[Cys-(tMeBn(CuDOTA-AET))-Pro-Pro-Thr-Gln-Phe-Cys]-OH (3BP-4293) of the following formula and
compound Hex-[Cys-(tMeBn(ZnDOTA-AET))-Pro-Pro-Thr-Gln-Phe-Cys]-OH (3BP-4343) of the following formula

Embodiment 10. The compound of any one of Embodiments 6 and 7, wherein the therapeutically active nuclide is a therapeutically active radionuclide.

Embodiment 11. The compound of Embodiment 10, wherein the therapeutically active radionuclide is selected from the group consisting of ⁴⁷Sc, ⁶⁷Cu, ⁸⁹Sr, ⁹⁰Y, ¹⁵³Sm, ¹⁴⁹Tb, ¹⁶¹Th, ¹⁷⁷Lu, ¹⁸⁶Re, ¹⁸⁸Re, ²¹²Pb, ²¹³Bi, ²²³Ra, ²²⁵Ac, ²²⁶Th, ²²⁷Th, ¹³¹I, ²¹¹At, preferably ⁴⁷Sc, ⁶⁷Cu, ⁹⁰Y, ¹⁷⁷Lu, ¹⁸⁸Re, ²¹²Pb, ²¹³Bi, ²²⁵Ac, ²²⁷Th, ¹³¹I, ²¹¹At and most preferably ⁹⁰Y, ¹⁷⁷Lu, ²²⁵Ac, ²²⁷Th, ¹³¹I and ²¹¹At.

Embodiment 12. The compound of any one of Embodiments 1 to 7, 10 to 11, wherein the compound interacts with a fibroblast activation protein (FAP), preferably with human FAP having an amino acid sequence of SEQ ID NO: 1 or a homolog thereof, wherein the amino acid sequence of the homolog has an identity of at least 85% to the amino acid sequence of SEQ ID NO: 1.

Embodiment 13. The compound of Embodiment 12, wherein the compound is an inhibitor of the fibroblast activation protein (FAP).

In an embodiment, the compound of the invention, as set out in the appended set of claims, is for use in a method for the diagnosis of a disease. In some embodiments, said method for the diagnosis is an imaging method. In some embodiments, said imaging method is selected from the group consisting of scintigraphy, Single Photon Emission Computed Tomography (SPECT) and Positron Emission Tomography (PET).

Embodiment 33. The compound of any one of Embodiments 1 to 7, 10 to 13, for use in a method for the treatment of a disease.

Embodiment 34. The compound for use of Embodiment 33, wherein the disease is a disease involving fibroblast activation protein (FAP), preferably upregulated expression of fibroblast activation protein (FAP).

Embodiment 35. The compound for use of any one of Embodiments 33 to 34, wherein the disease involves cells showing upregulated expression of fibroblast activation protein (FAP), preferably diseased tissue containing cells showing upregulated expression of fibroblast activation protein (FAP), more preferably disease involving tumor associated fibroblasts.

Embodiment 36. The compound for use of any one of Embodiments 33 to 35, wherein the disease is a neoplasm, preferably a cancer or tumor.

Embodiment 37. The compound for use of Embodiment 36, wherein the neoplasm, cancer, and tumor are each and individually selected from the group comprising a solid tumor, an epithelial tumor, bladder cancer, breast cancer, cervical cancer, colorectal cancer, cholangiocarcinoma, endometrial cancer, esophageal cancer, gastric cancer, gastrointestinal stromal tumors, head and neck cancer, liver cancer, lung cancer, melanoma, mesothelioma, neuroendocrine tumors and carcinomas, ovarian cancer, pancreatic cancer, prostate cancer, renal cell carcinoma, salivary carcinoma, sarcoma, squamous cell carcinoma, and thyroid cancer.

Embodiment 38. The compound for use of Embodiment 37, wherein the neoplasm, cancer, and tumor are each and individually selected from the group comprising breast cancer, colorectal cancer, cholangiocarcinoma, head and neck cancer, lung cancer, mesothelioma, neuroendocrine tumors and carcinomas, ovarian cancer, pancreatic cancer, prostate cancer, sarcoma, and squamous cell carcinoma.

Embodiment 39. The compound for use of any one of Embodiments 33 to 35, wherein the disease is selected from the groups comprising inflammatory disease, cardiovascular disease, autoimmune disease, and fibrotic disease.

Embodiment 40. The compound for use of Embodiment 39, wherein the disease is an inflammatory disease.

Embodiment 41. The compound for use of Embodiment 40, wherein the disease is atherosclerosis, arthritis, or rheumatoid arthritis.

Embodiment 42. The compound for use of Embodiment 39, wherein the disease is a cardiovascular disease.

Embodiment 43. The compound for use of Embodiment 42, wherein the diseases is a cardiovascular disease involving atherosclerotic plaques.

Embodiment 44. The compound for use of Embodiment 43, wherein the diseases is an atherosclerotic pathology caused by rupture of plaques, acute coronary syndrome, myocardial infarction, thrombosis, or vessel occlusion.

Embodiment 45. The compound for use of Embodiment 39, wherein the disease is a fibrotic disease.

Embodiment 46. The compound for use of Embodiment 45, wherein the disease is selected form the group comprising idiopathic pulmonary fibrosis, Crohn's disease, and liver fibrosis.

Embodiment 47. The compound for use of any one of Embodiments 33 to 38, wherein the compound comprises a therapeutically active nuclide, preferably a therapeutically active radionuclide.

Embodiment 48. The compound for use of Embodiment 47, wherein the therapeutically active nuclide is selected from the group comprising ⁴⁷Sc, ⁶⁷Cu, ⁸⁹Sr, ⁹⁰Y, ¹⁵³Sm, ¹⁴⁹Tb, ¹⁶¹Tb, ¹⁷⁷Lu, ¹⁸⁶Re, ¹⁸⁸Re, ²¹²Pb, ²¹³Bi, ²²³Ra, ²²⁵Ac, ²²⁶Th, ²²⁷Th, ¹³¹I, ²¹¹At, preferably ⁴⁷Sc, ⁶⁷Cu, ⁹⁰Y, ¹⁷⁷Lu, ¹⁸⁸Re, ²¹²Pb, ²¹³Bi, ²²⁵Ac, ²²⁷Th, ¹³¹I, ²¹¹At and most preferably ⁹⁰Y, ¹⁷⁷Lu, ²²⁵Ac, ²²⁷Th, ¹³¹I and ²¹¹At.

Embodiment 49. The compound for use of any one of Embodiments 33 to 48, wherein the method comprises the administration of a therapeutically effective amount of the compound to a subject, preferably to a mammal, wherein the mammal is selected from the group comprising man, companion animals, pets, and livestock, more preferably the subject is selected from the group comprising man, dog, cat, horse, and cow, and most preferably the subject is a human being.

Embodiment 99. A method for the treatment of a disease in a subject, wherein the method comprises administering to the subject a therapeutically effective amount of a compound according to any one of Embodiment 1 to 7, 10 to 13. Embodiment 100. The method of Embodiment 99, wherein the compound comprises a therapeutically active agent, whereby the agent is preferably a radionuclide.

Embodiment 101. The method of any one of Embodiments 99 to 100, wherein the disease is a disease involving fibroblast activation protein (FAP), preferably upregulated expression of fibroblast activation protein (FAP).

Embodiment 102. The method of any one of Embodiments 99 to 101, wherein the disease involves cells showing upregulated expression of fibroblast activation protein (FAP), preferably diseased tissue containing cells showing upregulated expression of fibroblast activation protein (FAP), more preferably disease involving tumor associated fibroblasts.

Embodiment 103. The method of any one of Embodiments 99 to 102, wherein the disease is selected from the groups comprising neoplasms, preferably cancers or tumors, and inflammatory disease, cardiovascular disease, autoimmune disease, and fibrotic disease.

Embodiment 104. A kit comprising a compound according to any one of Embodiments 1 to 7, 10 to 13, one or more optional excipient(s) and optionally one or more device(s), whereby the device(s) is/are selected from the group comprising a labeling device, a purification device, a handling device, a radioprotection device, an analytical device or an administration device.

More specifically, the problem underlying the present invention is solved in a first aspect by a compound selected from the group consisting of

• compound Hex-[Cys(tMeBn(DOTA-AET))-Pro-Pro-Thr-Gln-Phe-Cys]-OH (3BP-3554) of the following formula and
• compound Hex-[Cys(tMeBn(DOTA-PP))-Pro-Pro-Thr-Gln-Phe-Cys]-Asp-NH2 (3BP-3407) of the following formula

More specifically, the problem underlying the present invention is solved in a second aspect by the compound according to the first aspect, including any embodiment thereof, for use in a method for the diagnosis of a disease.

More specifically, the problem underlying the present invention is solved in a third aspect by the compound according to the first aspect, including any embodiment thereof, for use in a method for the treatment of a disease.

More specifically, the problem underlying the present invention is solved in a fourth aspect by the compound according to the first aspect, including any embodiment thereof, for use in a method for the identification of a subject, wherein the subject is likely to respond or likely not to respond to a treatment of a disease, wherein the method for the identification of a subject comprises carrying out a method of diagnosis using the compound according to the first aspect including any embodiment thereof.

More specifically, the problem underlying the present invention is solved in a fifth aspect by the compound according to the first aspect, including any embodiment thereof, for use in a method for the selection of a subject from a group of subjects, wherein the subject is likely to respond or likely not to respond to a treatment of a disease, wherein the method for the selection of a subject from a group of subjects comprises carrying out a method of diagnosis using the compound according to the first aspect, including any embodiment thereof.

More specifically, the problem underlying the present invention is solved in a sixth aspect by the compound according to the first aspect, including any embodiment thereof, for use in a method for the stratification of a group of subjects into subjects which are likely to respond to a treatment of a disease, and into subjects which are not likely to respond to a treatment of a disease, wherein the method for the stratification of a group of subjects comprises carrying out a method of diagnosis using the compound according to the first aspect, including any embodiment thereof.

More specifically, the problem underlying the present invention is solved in a seventh aspect by a composition, preferably a pharmaceutical composition, wherein the composition comprises a compound according to the first aspect including any embodiment thereof and a pharmaceutically acceptable excipient.

More specifically, the problem underlying the present invention is solved in an eighth aspect by a method for the diagnosis of a disease in a subject, wherein the method comprises administering to the subject a diagnostically effective amount of a compound according to the first aspect, including any embodiment thereof.

More specifically, the problem underlying the present invention is solved in a ninth aspect by a method for the treatment of a disease in a subject, wherein the method comprises administering to the subject a therapeutically effective amount of a compound according to the first aspect including any embodiment thereof.

More specifically, the problem underlying the present invention is solved in a tenth aspect by a kit comprising a compound according to the frist aspect, including any embodiment thereof, one or more optional excipient(s) and optionally one or more device(s), whereby the device(s) is/are selected from the group comprising a labeling device, a purification device, a handling device, a radioprotection device, an analytical device or an administration device.

It will be acknowledged by a person skilled in the art that a or the compound of the invention is any compound disclosed herein, including but not limited to any compound described in any of the above embodiments and any of the following embodiments.

It will be acknowledged by a person skilled in the art that a or the method of the invention is any method disclosed herein, including but not limited to any method described in any of the above embodiments and any of the following embodiments.

It will be acknowledged by a person skilled in the art that a or the composition of the invention is any composition disclosed herein, including but not limited to any composition described in any of the above embodiments and any of the following embodiments.

It will be acknowledged by a person skilled in the art that a or the kit of the invention is any kit disclosed herein, including but not limited to any kit described in any of the above embodiments and any of the following embodiments.

The present invention is based on the surprising finding of the present inventors that the compound of the invention and more specifically the cyclic peptide thereof provides for a highly specific binding of a compound comprising such cyclic peptide to fibroblast activation protein (FAP), since FAP-specific cyclic peptide-based inhibitors with nanomolar affinity have not been described so far.

Finally, the present inventors have found that the compounds of the invention are surprisingly stable in blood plasma, and are surprisingly useful as imaging agents and efficacious in shrinking tumors.

In an embodiment and as preferably used herein, a chelator is a compound which is capable of forming a chelate, whereby a chelate is a compound, preferably a cyclic compound where a metal or a moiety having an electron gap or a lone pair of electrons participates in the formation of the ring. More preferably, a chelator is this kind of compound where a single ligand occupies more than one coordination site at a central atom.

In an embodiment and as preferably used herein, a diagnostically active compound is a compound which is suitable for or useful in the diagnosis of a disease.

In an embodiment and as preferably used herein, a diagnostic agent or a diagnostically active agent is a compound which is suitable for or useful in the diagnosis of a disease.

In an embodiment and as preferably used herein, a therapeutically active compound is a compound which is suitable for or useful in the treatment of a disease.

In an embodiment and as preferably used herein, a therapeutic agent or a therapeutically active agent is a compound which is suitable for or useful in the treatment of a disease.

In an embodiment and as preferably used herein, a theragnostically active compound is a compound which is suitable for or useful in both the diagnosis and therapy of a disease.

In an embodiment and as preferably used herein, a theragnostic agent or a theragnostically active agent is a compound which is suitable for or useful in both the diagnosis and therapy of a disease.

In an embodiment and as preferably used herein, theragonstics is a method for the combined diagnosis and therapy of a disease; preferably, the combined diagnostically and therapeutically active compounds used in theragnostics are radiolabeled.

In an embodiment and as preferably used herein, treatment of a disease is treatment and/or prevention of a disease.

In an embodiment and as preferably used herein, a disease involving FAP is a disease where cells including but not limited to fibroblasts expressing, preferably in an upregulated manner, FAP and tissue either expressing FAP or containing or comprising cells such as fibroblasts, preferably expressing FAP in an upregulated manner respectively, are either a or the cause for the disease and/or the symptoms of the disease, or are part of the pathology underlying the disease. A preferred FAP-expressing cell is a cancer associated fibroblast (CAP). In an embodiment of the disease, preferably when used in connection with the treatment, treating and/or therapy of the disease, affecting the cells, the tissue and pathology, respectively, results in cure, treatment or amelioration of the disease and/or the symptoms of the disease. In an embodiment of the disease, preferably when used in connection with the diagnosis and/or diagnosing of the disease, labeling of the FAP-expressing cells and/or of the FAP-expressing tissue allows discriminating or distinguishing said cells and/or said tissue from healthy or FAP-non-expressing cells and/or healthy or FAP non-expressing tissue. More preferably such discrimination or distinction forms the basis for said diagnosis and diagnosing, respectively. In an embodiment thereof, labeling means the interaction of a detectable label either directly or indirectly with the FAP-expressing cells and/or with the FAP-expressing tissue or tissue containing such FAP-expressing cells; more preferably such interaction involves or is based on the interaction of the label or a compound bearing such label with FAP.

In an embodiment and as preferably used herein, a target cell is a cell which is expressing FAP and is a or the cause for a disease and/or the symptoms of a disease, or is part of the pathology underlying a disease.

In an embodiment and as preferably used herein, a non-target cell is a cell which is either not expressing FAP and/or is not a or the cause for a disease and/or the symptoms of a disease, or is part of the pathology underlying a disease.

In an embodiment and as preferably used herein, a neoplasm is an abnormal new growth of cells. The cells in a neoplasm grow more rapidly than normal cells and will continue to grow if not treated. A neoplasm may be benign or malignant.

In an embodiment and as preferably used herein, a tumor is a mass lesion that may be benign or malignant.

In an embodiment and as preferably used herein, a cancer is a malignant neoplasm.

The amino acid sequences of the peptides provided herein are depicted in typical peptide sequence format, as would be understood by the ordinary skilled artisan. For example, the three-letter code of a conventional amino acid, or the code for a non-conventional amino acid or the abbreviations for additional building blocks, indicates the presence of the amino acid or building block in a specified position within the peptide sequence. The code for each amino acid or building block is connected to the code for the next and/or previous amino acid or building block in the sequence by a hyphen which (typically represents an amide linkage).

Where an amino acid contains more than one amino and/or carboxy group all orientations of this amino acid are in principle possible, but in α-amino acid the utilization of the α-amino and the α-carboxy group is preferred and otherwise preferred orientations are explicitly specified.

For amino acids, in their abbreviations the first letter indicates the stereochemistry of the C-α-atom if applicable. For example, a capital first letter indicates that the L-form of the amino acid is present in the peptide sequence, while a lower case first letter indicating that the D-form of the correspondent amino acid is present in the peptide sequence.

In an embodiment and as preferably used herein, an aromatic L-α-amino acid is any kind of L-α-amino acid which comprises an aryl group.

In an embodiment and as preferably used herein, a heteroaromatic L-α-amino acid is any kind of L-α-amino acid which comprises a heteroaryl group.

Unless indicated to the contrary, the amino acid sequences are presented herein in N- to C-terminus direction.

Compounds of the invention typically contain amino acid sequences as provided herein. Conventional amino acids, also referred to as natural amino acids are identified according to their standard three-letter abbreviations and one-letter abbreviations, as set forth in Table 2. Amino acid 3-letter abbreviation 1-letter abbreviation Alanine Ala A Arginine Arg R Asparagine Asn N Aspartic acid Asp D Cysteine Cys C Glutamic acid Glu E Glutamine Gln Q Glycine Gly G Histidine His H Isoleucine Ile I Leucine Leu L Lysine Lvs K Methionine Met M Phenylalanine Phe F Proline Pro P Serine Ser S Threonine Thr T Tryptophan Trp W Tyrosine Tyr Y Valine Val V

Non-conventional amino acids, also referred to as non-natural amino acids, are any kind of non-oligomeric compound which comprises an amino group and a carboxylic group and is not a conventional amino acid.

Examples of non-conventional amino acids and other building blocks as used for the construction of compounds of the invention are identified according to their abbreviation or name found in Table 3. The structures of some building blocks are depicted with an exemplary reagent for introducing the building block into the peptide (e.g., as carboxylic acid like) or these building blocks are shown as residue which is completely attached to another structure like a peptide or amino acid. The structures of the amino acids are shown as explicit amino acids and not as residues of the amino acids how they are presented after implementation in the peptide sequence. Some larger chemical moieties consisting of more than one moiety are also shown for the reason of clarity. Abbreviation Name Structure 3MeBn 3-Methylbenzylidene AET 2-Aminoethanethiol CuDOTA DOTA complexing Copper Cy5SO3 Cy5 dye (mono S03) Cys(3MeBn) Cys(tMeBn (DOTA-AET)) Cys(tMeBn (DOTA-PP)) Cys(tMeBn (H-AET)) Cys(tMeBn (H-PP)) DOTA 1,4,7,10-Tetraazacyclododecane-1,4,7,10-tetraacetic acid EuDOTA DOTA complexing Europium GaDOTA DOTA complexing Gallium Hex Hexanoic acid Hex- hexanoyl InDOTA DOTA complexing Indium LuDOTA DOTA complexing Lutetium PP Piperazinyliden tMeBn 1,3,5-Trimethylbenzyliden tMeBn(H-AET) tMeBn(H-PP) ZnDOTA Zinc complex of DOTA

In accordance with the instant application, DOTA stands for 1,4,7,10-tetrazacyclododecane-1,4,7,10-tetraacetic acid.

It will be further acknowledged by the persons skilled in the art that the presence of a chelator in the compound of the invention includes, if not stated otherwise, the possibility that the chelator is complexed to any metal complex partner, i.e. any metal which, in principle, can be complexed by the chelator. An explicitly mentioned chelator of a compound of the invention or the general term chelator in connection with the compound of the invention refers either to the uncomplexed chelator as such or to the chelator to which any metal complex partner is bound, wherein the metal complex partner is any radioactive or non-radioactive metal complex partner. Preferably the chelator metal complex, i.e. the chelator to which the metal complex partner is bound, is a stable chelator metal complex.

Non-radioactive chelator metal complexes have several applications, e.g. for assessing properties like stability or activity which are otherwise difficult to determine. One aspect is that cold variants of the radioactive versions of the metal complex partner (e.g. non-radioactive Gallium, Lutetium or Indium complexes as described in the examples) can act as surrogates of the radioactive compounds. Furthermore, they are valuable tools for identifying metabolites in vitro or in vivo, as well as for assessing toxicity properties of the compounds of invention. Additionally, chelator metal complexes can be used in binding assays utilizing the fluorescence properties of some metal complexes with distinct ligands (e.g. Europium salts).

It will be acknowledged by a person skilled in the art that the radioactive nuclide which is or which is to be attached to the compound of the invention, is selected taking into consideration the disease to be treated and/or the disease to be diagnosed, respectively, and/or the particularities of the patient and patient group, respectively, to be treated and to be diagnosed, respectively.

In an embodiment of the present invention, the radioactive nuclide is also referred to as radionuclide. Radioactive decay is the process by which an atomic nucleus of an unstable atom loses energy by emitting ionizing particles (ionizing radiation). There are different types of radioactive decay. A decay, or loss of energy, results when an atom with one type of nucleus, called the parent radionuclide, transforms to an atom with a nucleus in a different state, or to a different nucleus containing different numbers of protons and neutrons. Either of these products is named the daughter nuclide. In some decays the parent and daughter are different chemical elements, and thus the decay process results in nuclear transmutation (creation of an atom of a new element). For example, the radioactive decay can be alpha decay, beta decay, and gamma decay. Alpha decay occurs when the nucleus ejects an alpha particle (helium nucleus). This is the most common process of emitting nucleons, but in rarer types of decays, nuclei can eject protons, or specific nuclei of other elements (in the process called cluster decay). Beta decay occurs when the nucleus emits an electron (β^--decay) or positron (β⁺-decay) and a type of neutrino, in a process that changes a proton to a neutron or the other way around. By contrast, there exist radioactive decay processes that do not result in transmutation. The energy of an excited nucleus may be emitted as a gamma ray in gamma decay, or used to eject an orbital electron by interaction with the excited nucleus in a process called internal conversion, or used to absorb an inner atomic electron from the electron shell whereby the change of a nuclear proton to neutron causes the emission of an electron neutrino in a process called electron capture (EC), or may be emitted without changing its number of proton and neutrons in a process called isomeric transition (IT). Another form of radioactive decay, the spontaneous fission (SF), is found only in very heavy chemical elements resulting in a spontaneous breakdown into smaller nuclei and a few isolated nuclear particles.

In a preferred embodiment of the present invention, the radionuclide can be used for labeling of the compound of the invention.

In an embodiment of the present invention, the radionuclide is suitable for complexing with a chelator, leading to a radionuclide chelate complex.

In a further embodiment one or more atoms of the compound of the invention are of non-natural isotopic composition, preferably these atoms are radionuclides; more preferably radionuclides of carbon, oxygen, nitrogen, sulfur, phosphorus and halogens: These radioactive atoms are typically part of amino acids, in some case halogen containing amino acids, and/or building blocks and in some cases halogenated building blocks each of the compound of the invention.

In a preferred embodiment of the present invention, the radionuclide has a half-life that allows for diagnostic and/or therapeutic medical use. Specifically, the half-life is between 1 min and 100 days.

In a preferred embodiment of the present invention, the radionuclide has a decay energy that allows for diagnostic and/or therapeutic medical use. Specifically, for γ-emitting isotopes, the decay energy is between 0.004 and 10 MeV, preferably between 0.05 and 4 MeV, for diagnostic use. For positron-emitting isotopes, the decay energy is between 0.6 and 13.2 MeV, preferably between 1 and 6 MeV, for diagnostic use. For particle-emitting isotopes, the decay energy is between 0.039 and 10 MeV, preferably between 0.4 and 6.5 MeV, for therapeutic use.

In a preferred embodiment of the present invention, the radionuclide is industrially produced for medical use. Specifically, the radionuclide is available in GMP quality.

In a preferred embodiment of the present invention, the daughter nuclide(s) after radioactive decay of the radionuclide are compatible with the diagnostic and/or therapeutic medical use. Furthermore, the daughter nuclides are either stable or further decay in a way that does not interfere with or even support the diagnostic and/or therapeutic medical use. Representative radionuclides which may be used in connection with the present invention are summarized in Table 4. Radionuclide Half-life (min) Half-life (hours) Half-life (days) Decay Energy (MeV) Additional decays (energy [MeV]) Carbon C-11 20.4 0.34 ECβ+ 1.982 Nitrogen N-13 9.97 0.17 ECβ+ 2.220 Oxygen O-15 2.00 ECβ+ 2.754 Fluorine F-18 110 1.83 β+ 1.656 Mg-28 20.9 β- 1.832 Aluminum Al-28 2.24 0.04 β- 4.642 Al-29 6.56 β- 3.690 Silicon Si-31 157 2.62 β- 1.492 Phosphorus P-30 2.50 0.04 β+ 4.232 P-32 14.3 β- 1.170 P-33 25.4 β- 0.077 Sulphur S-35 87.4 β- 0.167 S-37 5.00 0.08 S-38 2.80 β- 2.937 Chlorine Cl-34m1 32.0 0.53 EC 5.693 Cl-38 37.2 0.62 β- 4.917 Cl-39 55.6 0.93 β- 3.422 Scandium Sc-43 3.89 EC 2.221 Sc-44 3.97 β+ 0.632 Sc-44m1 58.6 2.44 IT 0.271 98.8% IT (0.27086), 1.2% EC (3.924) Sc-46 83.8 β- 2.367 Sc-47 80.4 3.35 β- 0.601 Sc-48 43.7 1.82 β- 3.988 Sc-49 57.4 0.96 β- 2.002 Titanium Ti-45 185 3.08 EC 2.062 Ti-51 5.76 β- 2.472 Vanadium V-47 32.6 0.54 β+ 2.931 V-48 16.2 EC 4.013 V-49 330 EC 0.602 V-52 3.74 β- 3.975 Chromium Cr-48 23.0 EC 1.655 Cr-49 42.1 0.70 β+ 2.628 Cr-51 27.7 EC 0.753 Cr-55 3.50 β- 2.603 Cr-56 5.94 β- 1.630 Manganese Mn-51 46.2 0.77 β+ 2.185 Mn-52m1 21.1 0.35 EC 5.091 98.25% EC (5.091), 1.75% IT (0.3796) Mn-52 5.59 β+ 3.689 Mn-54 312 EC 1.377 Mn-56 2.58 β- 3.696 Iron Fe-52 8.28 EC 2.375 Fe-53m1 2.54 IT 3.042 Fe-53 8.51 EC 3.742 Fe-59 44.5 β- 1.565 Fe-61 5.98 β- 3.977 Cobalt Co-55 17.5 EC 3.451 Co-56 78.8 EC 4.567 Co-57 271 EC 0.836 Co-58m1 9.15 IT 0.026 Co-58 70.8 EC 2.308 Co-60m1 10.5 0.17 IT 0.059 99.76% IT (0.05932), 0.24% β- (2.882) Co-61 1.65 β- 1.324 Co-62m1 13.9 0.23 β- 5.337 Nickel Ni-56 146 6.10 EC 2.133 Ni-57 36.1 1.50 β+ 3.262 Ni-63 β- 0.067 Ni-65 2.52 β- 2.138 Ni-66 54.6 2.28 β- 0.252 Copper Cu-60 23.2 0.39 EC 6.128 Cu-61 3.41 EC 2.238 Cu-62 9.74 0.16 EC 3.959 Cu-64 12.7 β+ 0.653 61.5% EC (1.674), 38.5% β- (0.5797) Cu-66 5.10 0.09 β- 2.641 Cu-67 2.58 β- 0.580 Cu-68m1 3.75 IT 0.722 84 % IT (0.72163), 16% β- (5.162) Cu-69 2.85 β- 2.681 Zinc Zn-60 2.38 EC 4.171 Zn-62 9.26 EC 1.620 Zn-63 38.1 0.64 EC 3.366 Zn-65 244 EC 1.352 Zn-69m1 13.8 IT 0.438 99.997% IT (0.43818), 0.003% β^- (1.348) Zn-69 57.0 0.95 β- 0.910 Zn-71m1 3.92 β- 2.970 99.95% β- (2.97), 0.05% IT (0.15986) Zn-71 2.45 β- 2.810 Zn-72 46.5 1.94 β- 0.443 Gallium Ga-65 15.2 0.25 EC 3.255 Ga-66 9.40 EC 5.175 Ga-67 78.2 3.26 EC 1.001 Ga-68 68.0 1.13 β+ 2.921 Ga-70 21.1 0.35 β- 1.652 99.59% β- (1.652), 0.41% EC (0.65456) Ga-72 14.1 β- 3.998 Ga-73 4.91 β- 1.598 Ga-74 8.12 0.14 β- 5.373 Selenium Se-70 41.0 0.68 β+ 2.412 Se-72 504 8.40 EC 0.362 Se-73m 39.0 0.65 IT 2.761 27.4% EC (2.761), 72.6 % IT (0.03608) Se-73 429 7.15 EC 2.725 Se-75 120 EC 0.865 Se-79m1 3.92 IT 0.096 99.94% IT (0.09622), 0.06% (0.247) Se-81m1 57.2 0.95 IT 0.103 99.95% IT (0.10253), 0.05% β- (1.689) Se-81 18.5 0.31 β- 1.587 Se-83 22.3 0.37 β- 3.673 Se-84 3.26 β- 1.836 Bromine Br-73 3.40 EC 4.580 Br-74m1 41.5 0.69 EC 9.921 Br-74 25.3 0.42 EC 6.925 Br-75 98.0 1.63 EC 3.062 Br-76 16.2 β+ 3.941 Br-77 57.0 2.38 β+ 0.342 Br-78 6.64 0.11 EC 3.574 99.99% EC (3.574), 0.01% β^- (0.72746) Br-80m1 265.20 4.42 IT 0.085 Br-80 17.40 0.29 EC 1.870 1,87 (EC), 2,004 (β-), EC = 91,7, β- = 8,3 Br-82 35.30 1.47 β- 3.090 Br-83 143.40 2.39 β- 0.972 Br-84 31.80 0.53 β- 4.656 Br-84m1 6.00 β- 4.960 Br-85 2.90 β- 2.905 Yttrium Y-83 7.08 EC 4.470 Y-83m1 2.85 EC 4.532 4.532 (ECβ+), 0.062 (IT), ECβ+ = 60, IT = 40 Y-84 Y-84m1 39.50 0.66 EC 6.490 Y-85 160.80 2.68 EC 3.250 Y-85m1 291.60 4.86 EC 3.270 Y-86m1 48.00 0.80 IT 0.218 Y-86 14.74 ECβ+ 4.22 Y-87m1 13.37 IT 0.381 0.381 (IT), 2.243 (ECβ+), IT = 98,43, ECβ+ = 1,57 Y-87 80.30 3.35 ECβ+ 1.862 Y-88 106.64 ECβ+ 3.623 Y-90m1 3.19 IT 0.682 Y-90 64.08 2.67 β- 2.280 Y-91m1 49.71 0.83 IT Y-91 58.51 β- Y-92 3.54 β- 3.639 Y-93 10.10 β- 2.893 Y-94 19.10 0.32 β- 4.919 Y-95 10.70 0.18 β- 4.420 Zirconium Zr-84 25.90 ECβ+ Zr-85 7.86 ECβ+ 4.690 Zr-86 16.50 ECβ+ 1.480 Zr-87 100.80 1.68 ECβ+ 3.665 Zr-88 83.40 EC 0.670 Zr-89m1 4.18 IT 0.588 3.420 (ECβ+), 0.588 (IT), ECβ+ = 6,23, IT = 93,77 Zr-89 78.43 3.27 β+ 0.9 Zr-95 63.98 β- 1.125 Zr-97 16.90 β- 2.658 Niobium Nb-87 2.60 ECβ+ 5.170 Nb-87m1 3.70 ECβ+ 5.170 Nb-88 14.50 0.24 ECβ+ 7.200 Nb-88m1 7.80 ECβ+ 7.200 Nb-89 114.00 1.90 ECβ+ 4.290 Nb-89m1 70.80 1.18 ECβ+ 4.290 Nb-90 14.60 ECβ+ 6.111 Nb-91m1 60.86 IT 0.104 0.104 (IT), 1.357 (ECβ+), IT = 93, ECβ+ = 7 Nb-95m1 86.60 3.61 IT 0.236 Nb-95 35.15 β- 0.926 Nb-96 23.35 β- 3.187 Nb-97 72.10 1.20 β- 1.934 Nb-98m1 51.50 0.86 β- 4.586 Molybdenum Mo-88 8.00 ECβ+ 3.720 Mo-89 2.04 ECβ+ 5.580 Mo-90 5.67 ECβ+ 2.489 Mo-91 15.49 ECβ+ 4.434 Mo-93m1 6.85 IT. ECβ+ 2.830 IT = 99.88, ECβ+ = 0.12 Mo-99 66.00 2.75 β- 1.375 Mo-101 14.62 0.24 β- 2.824 Mo-102 11.30 β- 1.010 Technetium Tc-91 3.14 0.05 ECβ+ 6.220 Tc-91m1 3.30 0.06 ECβ+ 6.570 6.57 (ECβ+), 0.35 (IT); ECβ+ ≈ 100, IT < 1 Tc-92 4.23 0.07 ECβ+ 7.870 Tc-93m1 43.50 0.73 IT 0.392 3.593 (ECβ+), 0.392 (IT), IT = 76.6, ECβ+ = 23.4 Tc-93 2.75 EC 3.201 Tc-94m1 52.00 0.87 β+ 2.36 1.730 (ECβ+), 0.075 (IT); ECβ+ ≈ 100, IT < 0.1 Tc-94 4.90 ECβ+ 4.256 Tc-95m1 61.00 ECβ+ 1.730 1.730 (ECβ+), 0.039 (IT); ECβ+ = 96.12, IT = 3.88 Tc-95 20.00 EC 1.691 Tc-96m1 51.50 0.86 IT 0.034 3.007 (ECβ+), 0.034 (IT), IT = 98.0, ECβ+ = 2.0 Tc-96 102.72 4.28 EC 2.973 Tc-97m1 87.00 IT 0.097 Tc-99m1 6.02 IT 0.143 Tc-101 14.20 0.24 β- 1.614 Tc-102m1 4.35 β- 4.530 4.53 (β-), 0.0 (IT), β- = 98, IT = 2 Tc-104 18.20 0.30 β- 5.600 Tc-105 7.60 0.13 β- 3.640 Ruthenium Ru-92 3.65 ECβ+ 4.500 Ru-94 51.80 0.86 EC 1.593 Ru-95 1.64 ECβ+ 2.572 Ru-97 69.60 2.90 EC 1.115 Ru-103 39.28 β- 0.763 Ru-105 4.44 β- 1.917 Ru-106 368.20 β- 0.039 Ru-107 3.76 0.06 β- 2.940 Ru-108 4.55 0.08 β- 1.360 Rhodium Rh-95 5.02 0.08 ECβ+ 5.110 Rh-95m1 1.96 0.03 IT 0.543 5.653 (ECβ+), 0.543 (IT); % ECβ+ = 12, IT = 88 Rh-96 9.90 0.17 ECβ+ 6.446 Rh-97 30.70 0.51 ECβ+ 3.520 Rh-97m1 46.20 0.77 ECβ+ 3.779 3.779 (ECβ+), 0.259 (IT); ECβ+ = 94.4, IT = 5.6 Rh-98 8.70 0.15 ECβ+ 5.057 Rh-98m1 3.50 0.06 ECβ+ 5.057 5.057 (ECβ+), 0.0 (IT); ECβ+ > 0 Rh-99m1 4.70 ECβ+ 2.167 2.167 (ECβ+), 0.064 (IT), ECβ+ > 99.84, IT < 0.16 Rh-99 16.00 ECβ+ 2.130 Rh-100 20.80 ECβ+ 3.630 Rh-101m1 104.16 4.34 EC 0.699 0.699 (EC), 0.157 (IT), EC = 92.8, IT = 7.2 Rh-102 207.00 ECβ+ 2.323 2.323 (ECβ+), 1.150 (β-), ECβ+ = 80, β- = 20 Rh-103m1 56.12 0.94 IT 0.040 Rh-104m1 4.34 IT 0.129 0.129 (IT), 2.570 (β-), IT = 99.87, β^- = 0.13 Rh-105 35.36 1.47 β- 0.567 Rh-106m1 132.00 2.20 β- 3.678 Rh-107 21.70 0.36 β- 1.511 Rh-108m1 6.00 β- 4.510 Palladium Pd-97 3.10 ECβ+ 4.800 Pd-98 17.70 ECβ+ 1.873 Pd-99 21.40 ECβ+ 3.365 Pd-100 87.12 3.63 EC 0.361 Pd-101 8.27 ECβ+ 1.980 Pd-103 16.96 EC 0.543 Pd-109 13.43 β- 1.116 Pd-109m1 4.70 IT 0.189 Pd-111 23.40 0.39 β- 2.190 Pd-111m1 5.50 IT 0.172 0.172 (IT), 2.362 (β^-); IT = 73, β- = 27 Pd-112 21.03 β- 0.288 Pd-114 2.42 0.04 β- 1.451 Silver Ag-100 2.01 ECβ+ 7.050 Ag-100m1 2.24 ECβ+ 7.066 7.066 (ECβ⁺), 0.015 (IT) Ag-101 11.10 ECβ+ 4.200 Ag-102 12.90 0.22 ECβ+ 5.920 Ag-102m1 7.70 ECβ+ 5.929 5.929 (ECβ+), 0.009 (IT), ECβ+ = 51, IT = 49 Ag-103 65.70 1.10 ECβ+ 2.688 Ag-104m1 33.50 0.56 ECβ+ 4.286 4.286 (ECβ+), 0.007 (IT), ECβ+ ≈ 100, IT < 0,07 Ag-104 69.20 1.15 ECβ+ 4.279 Ag-105 41.00 ECβ+ 1.346 Ag-106m1 201.84 8.41 EC 3.055 Ag-106 23.96 0.40 ECβ+ 2.965 2.965 (ECβ+), 0.195 (β-), ECβ+ = 99.5, β- < 1 Ag-108 2.37 0.04 β- 1.649 1.649 (β-), 1.918 (ECβ+), β- = 97.15, ECβ+ = 2.85 Ag-110m1 249.90 β- 3.010 3.010 (β-), 0.188 (IT), β^- = 98.64, IT = 1.,36 Ag-111 178.80 7.45 β- 0.810 Ag-112 187.20 3.12 β- 3.956 Ag-113 322.20 5.37 β- 2.016 Ag-115 20.00 0.33 β- 3.100 Ag-116 2.68 β- 6.160 Cadmium Cd-102 5.50 ECβ+ 2.587 Cd-103 7.30 ECβ+ 4.142 Cd-104 57.70 0.96 ECβ+ 1.136 Cd-105 55.50 ECβ+ 2.739 Cd-107 6.49 ECβ+ 1.417 Cd-111 48.54 IT 0.396 Cd-115m1 44.60 β- 1.627 Cd-115 53.46 2.23 β- 1.446 Cd-117m1 201.60 3.36 β- 2.653 Cd-117 149.40 2.49 β- 2.517 Cd-118 50.30 β- 0.520 Cd-119 2.69 β- 3.800 Cd-119m1 2.20 β- 3.947 Indium In-105 5.07 ECβ+ 4.85 In-106 6.20 ECβ+ 6.52 In-106m1 5.20 ECβ+ 6.55 In-107 32.40 ECβ+ 3.43 In-108 58.00 ECβ+ 5.15 In-108m1 39.60 ECβ+ 5.18 In-109 4.20 ECβ+ 2.020 In-110 4.9 ECβ+ 3.878 In-110m1 69.10 1.15 ECβ+ 3.940 In-111 67.92 2.83 EC 0.245 In-112 14.40 0.24 ECβ+ 2.586 2.586 (ECβ+), 0.664 (β-); ECβ+ = 56, β- = 44 In-113m1 1.66 IT 0.392 In-114m1 49.51 IT 0.190 0.190 (IT), 1.642 (ECβ+), IT = 96.75, ECβ+ = 3.25 In-115m1 4.49 IT 0.336 0.336 (IT), 0.831 (β-), IT = 95.0, β^- = 5.0 In-116m1 54.15 0.90 β- 3.401 In-117m1 116.50 1.94 β- 1.770 1.770 (β^-), 0.315 (IT); β-= 52.9, IT = 47.1 In-117 43.80 0.73 β- 1.455 In-118m1 4.45 β- 4.483 In-119m1 18.00 0.30 β- 2.675 2.675 (β^-), 0.311 (IT); β-= 94.4, IT = 5.6 In-119 2.40 0.04 β- 2.364 In-121m1 3.88 0.06 β- 3.674 3.674 (β-), 0.314 (IT), β^- = 98.8, IT = 1.2 Tin Sn-107 2.90 ECβ+ 5.01 Sn-108 10.30 ECβ+ 2.092 Sn-109 18.00 ECβ+ 3.85 Sn-110 4.11 EC 0.638 Sn-111 35.30 0.59 ECβ+ 2.445 Sn-113m1 21.40 ECβ+ 1.113 0.077 (IT), 1.113 (ECβ+), IT = 91.1, ECβ+ = 8.9 Sn-113 115.09 ECβ+ 1.036 Sn-117m1 13.61 IT 0.135 Sn-119m1 293.00 IT 0.090 Sn-121 27.06 1.13 β- 0.388 Sn-123m1 40.08 0.67 β- 1.429 Sn-123 129.20 β- 1.404 Sn-125 231.36 9.64 β- 2.364 Sn-125m1 9.52 β- 2.364 Sn-127 2.10 β- 3.20 Sn-127m1 4.13 β^- 3.21 Sn-128 59.10 0.99 β- 1.27 Sn-129 2.23 β^- 4.00 Sn-129m1 6.90 β^- 4.04 4.035 (β-), 0.035 (IT), β^- ≈ 100, IT ≈ 2·10^-4 Sn-130 3.72 β^- 2.15 Antimony Sb-113 6.67 0.11 β+ 3.905 Sb-114 3.49 0.06 β+ 5.880 Sb-155 32.10 0.54 β+ 3.030 Sb-116 15.80 0.26 β+ 4.707 Sb-116m1 60.30 1.01 β⁺ 5.090 Sb -117 62.80 2.80 β⁺ 1.757 Sb-118 3.60 0.06 β⁺ 3.657 Sb-18m1 5.00 β⁺ 3.907 Sb-119 38.19 1.59 EC 0.594 Sb-120m1 138.24 5.76 EC 2.681 Sb-120 15.89 0.26 ECβ+ 2.681 Sb-122 65.28 2.72 β- 1.979 1.979 (β-), 1.620 (ECβ+), β- = 97.59, ECβ+ = 2.41 Sb-122m2 4.19 0.07 IT 0.164 Sb-124m2 20.20 0.34 IT 0.037 Sb-124 60.20 β- 2.905 Sb-126m1 19.15 0.32 β- 3.688 3.688 ((3-), 0.016 (IT), β-= 86, IT = 14 Sb-126 12.40 β- 3.670 Sb-127 92.40 3.85 β- 1.581 Sb-128 9.01 β^- 4.380 Sb-128m1 10.40 0.17 β- 4.380 4.380 (β-), 0.0 (IT), β- = 96.4, IT = 3.6 Sb-129 259.20 4.32 β- 2.380 Sb-129m1 17.70 0.30 β- 4.231 4.231 (β-), 1.851 (IT), β-= 85, IT = 15 Sb-130 40.00 0.67 β- 4.960 Sb-130m1 6.30 0.11 β^- 4.960 Sb-131 23.00 0.38 β- 3.190 Sb-132 2.79 β- 5.290 Sb-132m1 4.15 0.07 β^- 5.290 Sb-133 2.50 0.04 β^- 4.003 Tellurium Te-112 2.00 ECβ+ 4.35 Te-114 15.20 ECβ+ 2.8 Te-115 5.80 ECβ+ 4.64 Te-115m1 6.70 ECβ+ 4.66 4.66 (ECβ+), 0.02 (IT), ECβ+ < 100 Te-116 2.49 EC 1.510 Te-117 62.00 1.00 ECβ+ 3.535 Te-118 360.00 6 EC 0.278 Te-119 961.80 16.03 ECβ+ 2.293 Te-119m1 282.00 4.7 ECβ+ 2.554 2.554 (ECβ+), 0.261 (IT), ECβ+ ≈ 100, IT < 0.008 Te-121m1 154.00 IT 0.294 0.294 (IT), 1.334 (ECβ+), IT = 88.6, ECβ+ = 11.4 Te-121 17.00 EC 1.040 Te-123m1 119.70 IT 0.248 Te-125m1 58.00 IT 0.145 Te-127m1 109.00 IT 0.088 0.088 (IT), 0.786 (β-), IT = 97.6, β^- = 2.4 Te-127 9.35 β^- 0.698 Te-129m1 33.60 IT 0.105 0.105 (IT), 1.604 (β-), IT = 63, β^- = 37 Te-129 69.60 1.16 β- 1.498 Te-131m1 30.00 1.25 β- 2.415 Te-131 25.00 0.42 β- 2.233 Te-132 78.20 3.26 β- 0.493 Te-133m1 55.40 0.92 β- 3.254 3.254 (β-), 0.334 (IT), β^- = 82.5, IT = 17.5 Te-133 12.45 0.21 β- 2.920 Te-134 41.80 0.70 β- 1.560 Iodine I-117 2.22 ECβ+ 4.67 I-118 13.70 ECβ+ 7.04 I-118m1 8.50 ECβ+ 7.14 7.144 (ECβ+), 0.104 (IT), ECβ+ < 100, IT > 0 I-119 19.10 ECβ+ 3.51 I-120m1 53.00 0.88 ECβ+ 5.615 I-120 81.00 1.35 ECβ+ 5.615 I-121 127.20 2.12 ECβ+ 2.270 I-122 3.62 0.06 ECβ+ 4.234 I-123 13.20 EC 0.159 I-124 100.32 4.18 β+ 2.14 I-125 59.408 EC 0.035 I-126 13.02 ECβ+ 2.155 2.155 (ECβ+), 1.258 (β-), ECβ+ = 56.3, β- = 43.7 I-128 24.99 0.42 β- 2.118 2118 (β-), 1.251 (ECβ+), β- = 93.1, ECβ+ = 6.9 I-130 12.36 β- 2.949 I-130m1 9.00 IT 0.040 0.040 (IT), 2.989 (β^-), IT = 84, β- = 16 I-131 192.96 8.04 β- 0.806 I-132m1 83.60 1.39 IT 0.120 0.120 (IT), 3.697 (β^-), IT = 86, β- = 14 I-132 2.30 β- 3.577 I-133 20.80 β- 1.770 I-134 52.60 0.88 β- 4.170 I-134m1 3.60 IT 0.316 0.316 (IT), 4.486 (β^-), IT = 97.7, β- = 2.3 I-135 6.61 β- 2.648 Lanthanum La-127 5.10 ECβ+ 4.69 La-127m1 3.70 ECβ+ 4.705 La-827 5.00 ECβ+ 6.7 La-129 11.60 ECβ+ 3.72 La-130 8.70 ECβ+ 5.6 La-131 59.00 0.98 ECβ+ 2.960 La-132 4.80 ECβ+ 4.710 La-132m1 24.30 IT 0.188 0.188 (IT), 4.898 (ECβ+), IT = 76, ECβ+ = 24 La-133 234.72 3.912 ECβ+ 2.23 La-134 6.67 0.11 ECβ+ 6.450 La-135 19.50 ECβ+ 1.200 La-136 9.87 ECβ+ 2.87 La-140 40.27 1.68 β- 3.762 La-141 3.93 β- 2.502 La-142 92.50 1.54 β- 4.505 La-143 14.23 0.24 β- 3.425 Cerium Ce-129 3.50 0.06 ECβ+ 5.05 Ce-130 25.00 0.42 ECβ+ 2.2 Ce-131 10.20 0.17 ECβ+ 4 Ce-131m1 5.00 ECβ+ 4 Ce-132 210.60 3.51 ECβ+ 1.29 1.29 (ECβ+), 2.341 (IT) Ce-133 97.00 1.62 ECβ+ 2.9 Ce-133m1 294.00 4.9 ECβ+ 2.937 Ce-134 72.00 3.00 EC 0.500 Ce-135 17.60 ECβ+ 2.026 Ce-137m1 34.40 1.43 IT 0.254 0.254 (IT), 1.476 (ECβ+), IT = 99.22, ECβ+ = 0.78 Ce-137 540.00 9.00 EC 1.222 Ce-139 137.66 EC 0.278 Ce-141 32.50 β- 0.581 Ce-143 33.00 1.38 β- 1.462 Ce-144 284.30 β- 0.319 Ce-145 3.01 β^- 2.54 Ce-146 13.52 β^- 1.04 Praseodymium Pr-133 6.50 ECβ+ 4.3 Pr-134 17.00 ECβ+ 6.2 Pr-134m1 11.00 ECβ+ 6.2 Pr-135 24.00 ECβ+ 3.72 Pr-136 13.10 0.22 ECβ+ 5.126 Pr-137 76.60 1.28 ECβ+ 2.702 Pr-138m1 2.10 ECβ+ 4.801 Pr-139 4.51 ECβ+ 2.129 Pr-140 3.39 ECβ+ 3.388 Pr-142m1 14.60 0.24 IT 0.004 Pr-142 19.12 β- 2.162 β- ≈ 100, EC = 0.0164 Pr-143 13.56 β- 0.934 Pr-144m1 7.20 0.12 IT 0.059 IT ≈ 100, β^- = 0.07 Pr-144 17.28 0.29 β- 2.997 Pr-145 5.98 β- 1.805 Pr-146 24.15 β^- 4.2 Pr-147 13.60 0.23 β- 2.69 Pr-148 2.27 β^- 4.93 Pr-148m1 2.00 β^- 5.02 Pr-149 2.26 β^- 3.397 Neodymium Nd-134 8.50 ECβ+ 2.77 Nd-135 12.40 ECβ+ 4.8 Nd-135m1 5.50 ECβ+ 4.856 Nd-136 50.65 0.84 ECβ+ 2.210 Nd-137 38.50 ECβ+ 3.69 Nd-138 302.40 5.04 EC 1.1 Nd-139m1 330.00 5.50 ECβ+ 3.021 3.021 (ECβ+), 0.231 (IT), ECβ+ = 88.2, IT = 11.8 Nd-139 29.70 0.50 ECβ+ 2.79 Nd-140 202.20 3.37 EC 0.222 Nd-141 2.49 ECβ+ 1.823 Nd-147 10.98 β- 0.896 Nd-149 1.73 β- 1.691 Nd-151 12.44 0.21 β- 2.442 Nd-152 11.40 β^- 1.11 Promethium Pm-137 2.40 ECβ+ Pm-138m1 3.24 ECβ+, IT 6.9 Pm-139 4.15 ECβ+ 4.52 Pm-140m1 5.95 ECβ+ 6.09 Pm-140m2 5.95 ECβ+ Pm-141 20.90 0.35 ECβ+ 3.715 Pm-143 265.00 EC 1.041 Pm-148m1 41.30 β- 2.606 2.606 (β-), 0.138 (IT), β-= 95.0, IT = 5.0 Pm-148 128.88 5.37 β- 2.468 Pm-149 53.08 2.21 β- 1.071 Pm-150 2.68 β- 3.454 Pm-151 28.40 1.18 β- 1.187 Pm-152 4.12 β^- 3.5 Pm-152m1 7.52 β^- 3.56 Pm-152m2 13.80 β^- β^- < 100, IT > 0 Pm-153 5.25 β^- 1.9 Pm-154m1 2.68 β^- 4.05 Samarium Sm-138 3.10 0.05 ECβ+ 3.900 Sm-139 2.57 0.04 ECβ+ 5.460 Sm-140 14.80 0.25 ECβ+ 3.020 Sm-141m1 22.60 0.38 ECβ+ 4.719 4.719 (ECβ+), 0.176 (IT); ECβ+ = 99.69, IT = 0.31 Sm-141 10.20 0.17 ECβ+ 4.543 Sm-142 72.49 1.21 ECβ+ 2.090 Sm-143 8.83 ECβ+ 3.443 Sm-145 340.00 EC 0.617 Sm-153 46.80 1.95 β- 0.810 Sm-155 22.30 0.37 β- 1.627 Sm-156 9.40 β- 0.722 Sm-158 5.30 0.09 β- 1.999 Europium Eu-143 2.63 ECβ+ 5.275 Eu-145 142.56 5.94 ECβ+ 2.660 Eu-146 110.64 4.61 ECβ+ 3.878 Eu-147 24.10 ECβ+ 1.722 Eu-148 54.50 ECβ+ 3.107 Eu-149 93.10 EC 0.692 Eu-150 12.62 β- 1.013 ECβ+ = 11, β- = 89 , IT < 5·10-8 Eu-152m 1 9.32 β- 1.865 ECβ+ = 28, β- = 72, 1.920 (ECβ+), 1.865 (β-) Eu-152m2 96.00 1.6 IT 0.148 Eu-154m1 46.30 0.77 IT 0.145 Eu-156 15.19 β- 2.451 Eu-157 15.15 β- 1.363 Eu-158 45.90 0.77 β- 3.490 Eu-159 18.10 β^- 2.514 Gadolinium Gd-144 4.50 ECβ+ 3.74 Gd-145 22.90 0.38 ECβ+ 5.050 Gd-146 48.30 EC 1.030 Gd-147 38.10 1.59 ECβ+ 2.187 Gd-149 225.60 9.40 ECβ+ 1.314 Gd-151 120.00 EC 0.464 Gd-153 242.00 EC 0.485 Gd-159 18.49 β- 0.971 Gd-161 3.66 β^- 1.956 Gd-162 8.40 β^- 1.39 Terbium Tb-147 1.65 ECβ+ 4.609 Tb-148 1.00 ECβ+ 5.690 Tb-148m1 2.20 ECβ+ 5.78 Tb-149 4.15 β+ 2.62 3.636 (ECβ+), 4.113 (α); ECβ+ = 83.3, α = 16.7 Tb-149m1 4.16 ECβ+ 3.672 3.672 (ECβ+), 4.077 (α), ECβ+ = 99.978 , α = 0.022 Tb-150 3.27 ECβ+ 4.656 Tb-150m1 5.80 ECβ+ 5.13 Tb-151 17.60 β+ 1.54 2.565 (ECβ+), 3.497 (α); ECβ+ ≈ 100, α = 9.5·10-3 Tb-152m1 4.20 IT 0.052 0.502 (IT), 4.492 (ECβ+), IT = 78.8, ECβ+ = 21.2 Tb-152 17.50 ECβ+ 3.990 3,.990 (ECβ+), 3.090 (α); ECβ+ ≈ 100, α < 7·10-7 Tb-153 56.16 2.34 ECβ+ 1.570 Tb-154 21.40 ECβ+ 3.560 3.56 (ECβ+), 0.25 (β-), ECβ+ ≈ 100, β- < 0.1 Tb-154m1 9.4 ECβ+ 3.560 3.56 (ECβ+), 0.0 (IT), 0.25 (β-), ECβ+ = 78.2, IT = 21.8, β- < 0.1 Tb-154m2 22.7 ECβ+ 3.560 3.56 (ECβ+), 0.0 (IT), ECβ+ = 98.2, IT = 1.8 Tb-155 127.68 5.32 EC 0.821 Tb-156m1 24.40 IT 0.050 Tb-156m2 5.00 IT 0.088 0.088 (IT), 2.532 (ECβ+) Tb-156 128.40 5.35 ECβ+ 2.444 2.444 (ECβ+), 0.434 (β-); ECβ+ ≈ 100, β- = ? Tb-160 72.30 β- 1.835 Tb-161 165.84 6.91 β- 0.593 Tb-162 7.60 0.13 β- 2.510 Tb-163 19.50 0.33 β- 1.785 Tb-164 3.00 β^- 3.89 Tb-165 2.11 β^- 3 Dysprosium Dy-148 3.10 186 ECβ+ 2.678 Dy-149 4.20 252 ECβ+ 3.812 Dy-150 7.17 430.2 ECβ+ 1.794 4.351 (α), 1.794 (ECβ+), α = 36, ECβ+ = 64 Dy-151 17.90 ECβ+ 2.870 2.87 (ECβ+), 4.180 (α), ECβ+ = 94.4, α = 5.6 Dy-152 2.38 ECβ+ 0.600 0.60 (ECβ+), 3.727 (α), EC(?) = 99.900, α = 0.100 Dy-153 6.4 ECβ+ 2.170 2.17 (ECβ+), 3.559 (α), ECβ+ ≈ 100, α = 0.0094 Dy-155 9.90 ECβ+ 2.095 Dy-157 8.14 ECβ+ 1.341 Dy-159 144.40 EC 0.366 Dy-165 2.33 β- 1.290 Dy-166 81.60 3.40 β- 0.486 Dy-167 6.20 β- 2.35 Dy-168 8.70 β- 1.6 Holmium Ho-153 2.01 ECβ+ 4.129 4.129 (ECβ+), 4.015 (α), ECβ+ = 99.949, α = 0.051 Ho-153m1 9.30 ECβ+ 4.179 4.179 (ECβ+), 4.119 (α), ECβ+ = 99.82, a = 0.18 Ho-154 11.76 ECβ+ 5.751 5.751 (ECβ+), 4.042 (α), ECβ+ = 99.981, α = 0.019 Ho-154m1 3.10 ECβ+ 6.071 6.071 (ECβ+), 4.362 (α), 0.320 (IT), ECβ+ ≈ 100, α < 0.001, IT ≈ 0 Ho-155 48.00 0.80 ECβ+ 3.102 Ho-156 56.00 0.93 ECβ+ 5.060 Ho-157 12.60 0.21 ECβ+ 2.540 Ho-158 11.30 ECβ+ 4.23 Ho-158m1 28.00 IT 0.067 4.297 (ECβ+), 0.067 (IT), ECβ+ < 19, IT > 81 Ho-158m2 21.30 ECβ+ 4.410 4.41 (ECβ+), 0.18 (IT), ECβ+ > 93, IT < 7 Ho-159 33.00 0.55 ECβ+ 1.838 Ho-160 25.60 ECβ+ 3.29 Ho-160m1 301.20 5.02 IT 0.060 0.06 (IT), 3.35 (ECβ+), IT = 65, ECβ+ = 35 Ho-161 150.00 2.50 EC 0.895 Ho-162m1 67.00 1.12 IT 0.106 0.106 (IT), 2.246 (ECβ+), IT = 62, ECβ+ = 38 Ho-162 15.00 0.25 ECβ+ 2.140 Ho-164m1 37.50 0.63 IT 0.140 Ho-164 29.00 0.48 EC 0.987 0.987 (EC), 0.962 (β-); EC = 60, β- = 40 Ho-166 26.80 1.12 β- 1.855 Ho-167 3.10 β- 1.007 Ho-168 2.99 β- 2.91 Ho-169 4.70 β- 2.124 Ho-170 2.76 β- 3.87 Erbium Er-154 3.73 ECβ+ 2.032 2.032 (ECβ+), 4.280 (α), ECβ+ = 99.53, α = 0.47 Er-155 5.30 ECβ+ 3.84 3.84 (ECβ+), 4.12 (α), ECβ+ = 99.978, α = 0.022 Er-156 19.50 ECβ+ 1.37 Er-157 18.65 ECβ+ 3.5 3.50 (ECβ+), 3.30 (α), ECβ+ ≈ 100, α < 0.02 Er-158 137.40 2.29 EC 0.9 Er-159 36.00 ECβ+ 2.769 Er-160 28.58 EC 0.33 Er-161 192.60 3.21 ECβ+ Er-163 75.00 1.25 ECβ+ 1.21 Er-165 621.60 10.36 EC 0.376 Er-169 223.20 9.30 β- 0.340 Er-171 451.20 7.52 β- 1.490 Er-172 49.30 2.05 β- 0.891 Er-174 3.30 β- 1.8 Thulium Tm-157 3.63 ECβ+ 4.48 Tm-158 3.98 ECβ+ 6.6 Tm-159 9.13 ECβ+ 3.85 Tm-160 9.40 ECβ+ 5.6 Tm-161 33.00 ECβ+ 3.16 Tm-162 21.70 0.36 ECβ+ 4.810 Tm-163 108.60 1.81 ECβ+ 2.439 Tm-164 2.00 ECβ+ 3.962 Tm-164m1 5.10 ECβ+ 3.962 Tm-165 30.06 ECβ+ 1.592 Tm-166 462.00 7.70 ECβ+ 3.040 Tm-167 221.76 9.24 EC 0.748 Tm-168 93.10 ECβ+ 1.679 1.679 (ECβ+), 0.257 (β-), ECβ+ = 99.990, β- = 0.010 Tm-170 128.60 β- 0.968 0.314 (ECβ+), 0.968 (β-), EC, β-(99%) Tm-172 63.60 2.65 β- 1.880 Tm-173 8.24 β- 1.298 Tm-174 5.40 β- 3.08 Tm-175 15.20 0.25 β- 2.39 Tm-176 1.90 β- 3.88 Ytterbium Yb-160 4.80 ECβ+ 2.3 Yb-161 4.20 ECβ+ 4.15 Yb-162 18.90 0.32 EC 1.660 Yb-163 11.05 ECβ+ 3.37 Yb-164 75.80 EC 1 Yb-165 9.90 ECβ+ 2.762 Yb-166 56.70 2.36 EC 0.304 Yb-167 17.50 0.29 ECβ+ 1.954 Yb-169 32.01 EC 0.909 Yb-175 100.56 4.19 β- 0.47 Yb-177 1.90 β- 1.399 Yb-178 74.00 1.23 β- 0.645 Yb-179 8.00 β- 2.4 Yb-180 2.40 β- Lutetium Lu-162m2 1.90 ECβ+ Lu-164 3.14 ECβ+ 6.25 Lu-165 10.74 ECβ+ 3.92 Lu-166 2.65 ECβ+ 5.48 Lu-166m2 2.12 ECβ+ 5.523 5.523 (ECβ+), 0.043 (IT),ECβ+ > 80, IT < 20 Lu-167 51.50 0.86 ECβ+ 3.130 Lu-168 5.50 ECβ+ 4.48 Lu-168m1 6.70 ECβ+ 4.700 4.70 (ECβ+), 0.220 (IT), ECβ+ > 95, IT < 5 Lu-169 34.06 1.42 ECβ+ 2.293 Lu-170 48.00 2.00 ECβ+ 3.459 Lu-171 197.28 8.22 ECβ+ 1.479 Lu-172 160.80 6.70 ECβ+ 2.519 Lu-174m1 142.00 IT 0.171 0.171 (IT), 1.545 (EC), IT = 99.38, EC = 0.62 Lu-176m1 3.68 β- 1.316 1.316 (β-), 0.229 (EC), β-= 99.905, EC = 0.095 Lu-177m1 160.90 β- 1.468 1.468 (β-), 0.970 (IT), β-= 78.3, IT = 21.7 Lu-177 6.71 β- 0.490 Lu-178m1 22.70 0.38 β- 2.219 Lu-178 28.40 0.47 β- 2.099 Lu-179 4.59 β- 1.405 Lu-180 5.70 β- 3.1 Lu-181 3.50 β- 2.5 Lu-182 2.00 β- Hafnium Hf-166 6.77 ECβ+ 2.3 Hf-167 2.05 ECβ+ 4 Hf-168 25.95 ECβ+ 1.8 Hf-169 3.24 ECβ+ 3.27 Hf-170 16.01 EC 1.1 Hf-171 12.1 ECβ+ 2.4 Hf-173 23.60 0.98 ECβ+ 1.610 Hf-175 70.00 EC 0.686 Hf-177m1 51.40 0.86 IT 2.740 Hf-179m2 25.10 IT 1.106 Hf-180m1 5.50 IT 1.141 1.141 (IT), 1.287 (β-), IT = 99,.7, β- = 0.3 Hf-181 42.40 β- 1.027 Hf-182m1 61.50 1.03 β- 1.546 1.546 (β-), 1.173 (IT), β- = 58, IT = 42 Hf-183 64.00 1.07 β- 2.010 Hf-184 4.12 β- 1.340 Hf-185 3.50 β- Tantalum Ta-168 2.00 ECβ+ 6.7 Ta-169 4.90 ECβ+ 4.44 Ta-170 6.76 ECβ+ 6 Ta-171 23.30 ECβ+ 3.7 Ta-172 36.80 0.61 ECβ+ 4.920 Ta-173 3.65 ECβ+ 2.790 Ta-174 1.20 ECβ+ 3.850 Ta-175 10.50 ECβ+ 2.000 Ta-176 8.08 ECβ+ 3.110 Ta-177 56.60 2.36 EC 1.166 Ta-178m1 2.36 EC 1.910 Ta-178 9.31 0.16 EC 1.910 Ta-180 8.15 EC 0.854 0.854 (EC), 0.708 (β-), EC = 86, β- = 14 Ta-182m1 15.84 0.26 IT 0.52 Ta-182 115.00 β- 1814.000 Ta-183 122.40 5.10 β- 1.070 Ta-184 8.70 β- 2.870 Ta-185 49.00 0.82 β- 1.992 Ta-186 10.50 0.18 β- 3.000 Tungsten W-170 2.42 ECβ+ 3 W-171 2.38 ECβ+ 4.6 W-172 6.60 ECβ+ 2.5 W-173 7.60 ECβ+ 4 W-174 31.00 ECβ+ 1.9 W-175 35.20 ECβ+ 2.91 W-176 2.50 EC 0.790 W-177 135.00 2.25 ECβ+ 2.000 W-178 21.70 EC 0.091 W-179m1 6.40 IT 0.222 0.222 (IT), 1.282 (ECβ+), IT = 99.72, ECβ+ = 0.28 W-181 121.20 EC 0.188 W-185 75.10 β- 0.433 W-187 23.72 0.99 β- 1.311 W-188 69.40 β- 0.349 W-189 11.50 β- 2.5 W-190 30.00 β- 1.27 Rhenium Re-173 1.98 ECβ+ 4.8 Re-174 2.40 ECβ+ 6.5 Re-175 5.89 ECβ+ 4.3 Re-176 5.30 ECβ+ 5.6 Re-177 14.00 0.23 ECβ+ 3.400 Re-178 13.20 0.22 ECβ+ 13.200 Re-179 19.50 ECβ+ 2.71 Re-180 2.43 0.04 ECβ+ 3.800 Re-181 20.00 ECβ+ 1.739 Re-182 64.00 EC 2.800 Re-182m1 12.70 ECβ+ 2.800 Re-183 70.00 EC 0.556 Re-184m1 169.00 IT 0.188 0.188 (IT), 1.671 (EC), IT = 75.4, EC = 24.6 Re-184 38.00 ECβ+ 1.483 Re-186 90.48 3.72 β- 1.07 0.582 (EC), 1.069 (β-); EC = 7.47, β- = 92.53 Re-188m1 18.60 0.31 IT 0.172 Re-188 16.98 β- 2.120 Re-189 24.30 1.01 β- 1.009 Re-190 3.10 β- 3.15 Re-190m1 192.00 3.2 β- 3.269 3.269 (β-), 0.119 (IT), β-= 54.4, IT = 45.6 Re-191 9.80 β- 2.045 Osmium Os-176 3.60 ECβ+ 3.2 Os-177 2.80 ECβ+ 4.5 Os-178 5.00 ECβ+ 2.3 Os-179 6.50 ECβ+ 3.68 Os-180 22.00 0.37 ECβ+ 1.470 Os-181 105.00 1.75 ECβ+ 2.930 Os-181m1 2.70 ECβ+ 2.979 Os-182 22.00 EC 0.91 Os-183 13.00 ECβ+ 2.13 Os-183m1 9.90 ECβ+ 2.301 2.301 (ECβ+), 0.171 (IT), ECβ+ = 85, IT = 15 Os-185 94.00 EC 1.013 Os-189m1 6.00 IT 0.031 Os-190m1 9.90 0.17 IT 1.705 Os-191m1 13.03 IT 0.074 Os-191 15.40 β- 0.314 Os-193 30.00 1.25 β- 1.140 Os-195 6.50 β- 2 Os-196 34.90 β- 1.16 Iridium Ir-181 4.90 ECβ+ 4.07 Ir-182 15.00 0.25 ECβ+ 5.61 Ir-183 58.00 ECβ+ 3.45 Ir-184 3.02 ECβ+ 4.600 Ir-185 14.00 ECβ+ 2.370 Ir-186 15.80 ECβ+ 3.831 Ir-186m1 1.90 ECβ+ 3.831 3.831 (ECβ+), 0 (IT), ECβ+ ≈ 75, IT ≈ 25 Ir-187 10.50 EC 1.502 Ir-188 41.50 1.73 ECβ+ 2.809 Ir-189 13.30 EC 0.532 Ir-190m2 3.25 ECβ+ 2.149 2.149 (ECβ+), 0.140 (IT), ECβ+ = 94.4, IT = 5.6 Ir-190m1 1.20 IT 0.026 Ir-190 12.10 ECβ+ 2.000 Ir-192 73.83 β- 1.460 1.46 (β-), 1.046 (EC), β-= 95.24, EC = 4.76 Ir-193m1 10.53 IT 0.08 Ir-194m1 171.00 β- 2.437 Ir-194 19.15 β- 2.247 Ir-195m1 3.80 β- 1.220 1.22 (β-), 0.10 (IT), β- = 95, IT = 5 Ir-195 2.50 β- 1.120 Ir-196m1 84.00 1.4 β- 3.620 Ir-197 5.80 β- 2.155 Ir-197m1 8.90 β- 2.270 2.27 (β-), 0.115 (IT), β- = 99.75, IT = 0.25 Platinum Pt-182 3.00 ECβ+ 2.850 2.85 (ECβ+), 4.943 (α), ECβ+ = 99.969, α = 0.031 Pt-183 6.50 ECβ+ 4.600 Pt-184 17.30 ECβ+ 2.300 Pt-185 70.90 1.1817 ECβ+ 3.800 Pt-185m1 33.00 ECβ+ 3.903 3.903 (ECβ+), 0.103 (IT), 4.643 (α), ECβ+ = 99, IT < 2 Pt-186 2.00 ECβ+ 1.380 Pt-188 10.20 EC 0.507 Pt-187 2.35 ECβ+ 3.11 Pt-189 10.87 ECβ+ 1.971 Pt-191 67.20 2.80 EC 1.019 Pt-193m1 103.92 4.33 IT 0.150 Pt-195m1 96.48 4.02 IT 0.259 Pt-197m1 95.41 1.59 IT 0.399 0.399 (IT) 1.119 (β-), IT = 96.7, β- = 3.3 Pt-197 18.30 β- 0.719 Pt-199 30.80 0.51 β- 1.702 Pt-200 12.50 β- 0.660 Pt-201 2.50 β- 2.66 Pt-202 44 β- Gold Au-185 4.25 ECβ+ 4.71 4.71 (ECβ+), 5.18 (α), ECβ+ = 99.74, α = 0.26 Au-185m1 6.80 ECP+ 4.71 Au-186 10.70 ECβ+ 6.04 Au-187 8.40 ECβ+ 3.6 3,6 (ECβ+), 4,79 (α), ECβ+ = 99,997, α = 0,003 Au-188 8.84 ECβ+ 5.3 Au-189 28.70 ECβ+ 2.85 ECβ+ ≈ 100, α < 3.10-5 Au-189m1 4.59 ECβ+ 3.097 ECβ+ ≈ 100, IT > 0 Au-190 42.80 ECβ+ 4.442 ECβ+ ≈ 100, α < 1.10-6 Au-191 3.18 ECβ+ 1.83 Au-192 4.94 ECβ+ 3.516 Au-193 17.65 EC 1.069 Au-194 398.02 16.58 ECβ+ 2.492 Au-195 183.00 EC 0.227 Au-196 148.39 6.18 ECβ+ 1.500 1.506 (ECβ+), 0.686 (β-), ECβ+ = 92.80, β- = 7.20 Au-196m2 9.60 IT 0.596 Au-198m1 55.20 2.30 IT 0.812 Au-198 64.70 2.70 β- 1.372 Au-199 75.34 3.14 β- 0.453 Au-200m1 18.70 β- 3.202 3.202 (β-), 0.962 (IT), β-= 82, IT = 18 Au-200 48.40 0.81 β- 2.240 Au-201 26.40 0.44 β- 1.275 Thallium Tl-189 2.30 ECβ+ 5.18 TI-190 2.60 ECβ+ 7 TI-190m1 3.70 ECβ+ 7 TI-191 ECβ+ 4.49 TI-191m1 5.22 ECβ+ 4.789 TI-192 9.60 ECβ+ 6.12 TI-192m1 10.80 ECβ+ 6.12 TI-193 21.60 ECβ+ 3.64 TI-193m1 2.11 IT 0.365 0.365 (IT), 4.005 (ECβ+), IT = 75, ECβ+ = 25 TI-194m1 32.80 0.55 ECβ+ 5.280 TI-194 33.00 0.55 EC 5.280 TI-195 1.16 ECβ+ 2.810 TI-196 1.84 ECβ+ 4.38 TI-196m1 1.41 ECβ+ 4.774 4.774 (ECβ+) 0.394 (IT), ECβ+ = 95.5, IT = 4.5 TI-197 2.84 ECβ+ 2.180 TI-198m1 1.87 ECβ+ 4.004 4.004 (ECβ+), 0.544 (IT), ECβ+ = 54, IT = 46 TI-198 5.30 ECβ+ 3.460 TI-199 7.42 ECβ+ 1.440 TI-200 26.10 1.09 ECβ+ 2.456 TI-201 3.04 EC 0.483 TI-202 12.23 ECβ+ 1.365 TI-206 4.20 0.07 β- 1.533 TI-206m1 3.74 IT 2.643 TI-207 4.77 0.08 β- 1.423 TI-208 3.07 0.05 β- 5.001 TI-209 2.20 0.04 β- 3.980 Lead Pb-191m1 2.10 ECβ+ 6.038 Pb-192 3.50 ECβ+ 3.400 3.4 (ECβ+), 5.221 (α), ECβ+ = 99.9941, α = 0.0059 Pb-193 2.00 ECβ+ Pb-193m1 5.80 ECβ+ 5.200 Pb-194 12.00 ECβ+ 2.700 Pb-195 15.00 ECβ+ 4.500 Pb-195m1 15.80 0.26 ECβ+ 4.500 Pb-196 37.00 ECβ+ 2.050 2.05 (ECβ+), 4.2 (a), ECβ+ ≈ 100, α < 3.10-5 Pb-197 8.00 ECβ+ 3.58 Pb-197m1 43.00 ECβ+ 3.889 3.889 (ECβ+), 0.319 (IT), ECβ+ = 81, IT = 19 Pb-198 2.40 ECβ+ 1.410 Pb-199 90.00 1.50 ECβ+ 2.880 Pb-199m1 12.20 IT 0.425 0.425 (IT), 3.305 (ECβ+), IT = 93, ECβ+ = 7 Pb-200 21.50 EC 0.811 Pb-201 9.33 ECβ+ 1.900 Pb-202m1 3.53 IT 2.710 Pb-203 51.87 2.16 EC 0.975 Pb-204m1 67.20 1.12 IT 2.186 Pb-209 3.25 β- 0.644 Pb-211 36.10 0.60 β- 1.373 Pb-212 10.64 β- 0.574 Pb-213 10.20 0.17 β- 2.070 Pb-214 26.80 0.45 β- 1.024 Bismuth Bi-197 9.33 ECβ+ 5.200 5.2 (ECβ+), 5.39 (α), ECβ+ ≈ 100, α = 1·10-4 Bi-197m1 5.04 α 5.890 5.89 (α), 5,7 (ECβ+), 0.50 (IT), α = 55, ECβ+ = 45, IT < 0.3 Bi-198 10.30 ECβ+ 6.56 Bi-198m1 11.60 ECβ+ 6.56 Bi-199 27.00 ECβ+ 4.34 Bi-199m1 24.70 ECβ+ 5.020 5.02 (ECβ+), 5.64 (α), 0.68 (IT), ECβ+ = 99, α≈ 0.01, IT < 2 Bi-200 36.40 ECβ+ 5.89 Bi-200m1 31.00 ECβ+ 5.89 ECβ+ > 90, IT < 10 Bi-201 108.00 1.80 EC 3.84 Bi-201m1 59.10 0.99 EC 4.686 4.686 (EC), 5.346 (IT), 5.346 (α), EC > 93, IT < 6.8, α≈ 0.3 Bi-202 1.67 ECβ+ 5.150 5.15 (ECβ+), 4.29 (α), ECβ+ ≈ 100, α < 1·10-5 Bi-203 11.76 ECβ+ 3.253 3.253 (ECβ+), 4.15 (α), ECβ+ ≈ 100, α ≈ 1·10-5 Bi-204 11.22 ECβ+ 4.438 Bi-205 15.31 ECβ+ 2.708 Bi-206 149.83 6.24 ECβ+ 3.758 Bi-210 120.29 5.01 β- 1.163 Bi-211 2.14 0.04 α 6.751 6.751 (α), 0.579 (β-), α = 99.724, β- = 0.276 Bi-212 60.55 1.01 β- 2.254 2.254 (β-), 6.207 (α), 11.208 (β^-+α); β- = 64.06, α = 35.94 Bi-212m1 25.00 α 6.457 6.457 (α), 2.504 (β-), α = 67, β^- = 33, β^-α = 30 Bi-212m2 7.00 β- 4.164 Bi-213 45.6 0.76 α 5.98 1.464 (β^-), 5.982 (α); β- = 97.91, α = 2.09 Bi-214 19.90 0.33 β- 3.272 3.272 (β^-), 5.617 (α); β- = 99.979, α = 0.021 Bi-215 7.60 β- 2.25 Bi-216 3.60 β- 4 Polonium Po-199 5.48 ECβ+ 5.600 5.6 (ECβ+), 6.074 (α), ECβ+ = 88, α = 12 Po-199m1 4.13 ECβ+ 5.910 5.91 (ECβ+), 6.384 (α), 0.310 (IT), ECβ+ = 59, α = 39, IT = 2.1 Po-200 11.50 ECβ+ 3.350 3.35 (ECβ+), 5.982 (α), ECβ+ = 88.9, α = 11.1 Po-201 15.30 ECβ+ 4.880 4.88 (ECβ+), 5.799 (α), ECβ+ = 98.4, α = 1.6 Po-201m1 8.90 IT 0.424 0.424 (IT), 5.304 (ECβ+), 6.223 (α), IT = 56, EC = 41, α ≈ 2.9 Po-202 44.70 0.75 ECβ+ 2.820 2.82 (ECβ+), 5.701 (α), ECβ+ = 98.08, a = 1.92 Po-203 36.70 0.61 ECβ+ 4.230 4.23 (ECβ+), 5.496 (α), ECβ+ = 99.89, a = 0.11 Po-204 3.53 ECβ+ 2.340 2.34 (ECβ+), 5.485 (α), ECβ+ = 99.34, α = 0.,66 Po-205 1.66 ECβ+ 3.530 3.53 (ECβ+), 5.324 (α), ECβ+ = 99.96, α = 0.04 Po-206 8.8 ECβ+ 1.846 1.846 (ECβ+), 5.326 (α), ECβ+ = 94.55, α = 5.45 Po-207 5.8 ECβ+ 2.909 2.909 (ECβ+), 5.216 (α), ECβ+ = 99.979, α = 0.021 Po-210 138.38 α 5.307 Po-218 3.05 0.05 α 6.115 6.115 (α), 0.265 (β-), α = 99.980 , β^- = 0.020 Astatine At-203 7.40 ECβ+ 5.060 5.06 (ECβ+), 6.21 (α), ECP+ = 69, α = 31 At-204 9.20 ECβ+ 6.480 6.48 (ECβ+), 6.07 (α), ECβ+ = 96.2 , α=3.8 At-205 26.20 0.44 ECβ+ 4.540 4.54 (ECβ+), 6.02 (α), ECβ+ = 90, α = 10 At-206 30.00 0.50 ECβ+ 5.720 5.72 (ECβ+), 5.888 (α), ECβ+ = 99.11, α = 0.89 At-207 1.80 ECβ+ 3.910 3.91 (ECβ+), 5.873 (α), ECβ+ = 91.4, α = 8.6 At-208 1.63 ECβ+ 4.973 4.973 (ECβ+), 5.751 (α), ECβ+ = 99.45, α = 0.55 At-209 5.41 ECβ+ 3.486 3.486 (ECβ+), 5.757 (α), ECβ+ = 95.9, α = 4.1 At-210 8.1 ECβ+ 3.981 3.981 (ECβ+), 5.631 (α), ECβ+ = 99.825, α = 0.175 At-211 7.21 α+ 5.98 0.786 (ECβ+), 5.982 (α), EC = 58.2, α = 41.8 At-220 3.71 β- α = 8, β- = 92, 3.65 (ECβ+), 6.05 (α) At-221 2.30 β- Radon Rn-205 2.80 ECβ+ 5.240 5.24 (ECβ+), 6.39 (α), ECβ+ = 77, α = 23 Rn-206 5.67 α 6.384 6.384 (α), 3.,31 (ECβ+), α = 63, ECβ+ = 37 Rn-207 9.25 ECβ+ 4.610 4.61 (ECβ+), 6.251 (α), ECβ+ = 79, α = 21 Rn-208 24.35 0.41 α 6.260 6.26 (α), 2.85 (ECβ+),α = 62, ECβ+ = 38 Rn-209 28.50 0.48 ECβ+ 3.930 3.93 (ECβ+), 6.155 (α), ECβ+ = 83, α = 17 Rn-210 2.40 α 6.159 6.159 (α), 2.374 (ECβ+), α = 96, ECβ+ = 4 Rn-211 14.60 EC 2.892 2.892 (ECβ+), 5.965 (α), EC = 72.6, α = 27.4 Rn-212 23.90 0.40 α 6.385 Rn-221 25.00 β- 1.220 1.22 (β-), 6.146 (α), β^- = 78, α=22 Rn-222 3.82 α 5.590 Rn-223 23.20 β- β^- ≈ 100, α = 0.0004 Rn-224 107.00 β- 0.8 Rn-225 4.50 β^- Rn-226 7.40 β^- 1.4 Francium Fr-210 3.18 α 6.700 6.7 (α), 6.262 (ECβ+), α = 60, ECβ+ = 40 Fr-211 3.10 α 6.660 6.66 (α), 4.605 (ECβ+), α > 80, EC < 20 Fr-212 20.00 0.33 ECβ+ 5.117 5.117 (ECβ+), 6.529 (α), ECβ+ = 57, α = 43 Fr-221 4.80 0.08 α 6.458 α ≈ 100, β^- = ?, ¹⁴C = 8.8·10 Fr-222 14.40 0.24 β- 2.033 Fr-223 21.80 0.36 β- 1.149 Fr-224 3.33 β- 2.83 Fr-225 4.00 β- 1.866 Fr-227 2.47 β- 2.49 Radium Ra-213 2.74 α 6.859 6.859 (α), 3.88 (ECβ+), α = 80, ECβ+ = 20 Ra-223 11.43 α 5.979 Ra-224 87.84 3.66 α 5.789 Ra-225 14.80 β- 0.357 Ra-227 42.20 0.70 β- 1.325 Ra-229 4.00 β^- 1.76 Ra-230 93.00 1.55 β- 0.990 Actinium Ac-223 2.10 0.04 α 6.783 Ac-224 2.90 α 1.403 1.403 (EC), 6.327 (α), 0.232 (β-), EC = 90.9, α = 9.1, β- < 1.6 Ac-225 10.00 α 5.935 Ac-226 29.00 1.21 β- 1.117 1.117 (β^-), 0.64 (EC), 5.563 (α), β- ≈ 83, EC = 17, α = 6·10-3 Ac-228 6.13 β- 2.127 Ac-229 62.70 β^- 1.1 Ac-231 7.50 β^- 2.1 Thorium Th-225 8.72 α 6.922 6.922 (α), 0.675 (EC), α ≈ 90, EC ≈ 10 Th-226 30.90 0.52 α 6.451 Th-227 18.72 α 6.051 Th-231 25.52 1.06 β- 0.389 Th-233 22.30 β^- 1.245 Th-234 24.10 β- 0.273 Th-235 7.10 β^- 1.93 Th-236 37.00 0.62 β^- Th-237 5.00 β^- Protactinium Pa-227 38.30 0.64 α 6.580 6.580 (α), 1.019 (EC), α = 85, EC = 15 Pa-228 22.00 ECβ+ 2.148 2.148 (ECβ+), 6.265 (α), ECβ+ = 98.0, α = 2.0 Pa-229 36.00 1.50 EC 0.316 Pa-230 17.40 ECβ+ 1.310 1.310 (ECβ+), 0.563 (β-), 5.439 (α), ECβ+ = 91.6, β- = 8.4, α = 0.0032 Pa-232 31.44 1.31 β- 1337.000 Pa-233 27.00 β- 0.571 Pa-234 6.70 β- 2.197 Pa-235 24.50 β^- 1.41 Pa-236 9.10 β^- 2.9 Pa-237 8.70 β^- 2.25 Pa-238 2.30 β^- 3.46 Uranium U-228 9.10 α 6.801 6.804 (α), 0.307 (EC), α > 95, EC < 5 U-229 58.00 0.97 ECβ+ 1.309 1.309 (ECβ+), 6.475 (α), ECβ+ ≈ 80, α ≈ 20 U-230 20.80 α 5.993 U-231 100.80 4.20 EC 0.360 U-235m1 25.00 IT U-237 162.00 6.75 β- 0.519 U-239 23.54 0.39 β- 1.265 U-240 14.10 β- 0.338 U-242 16.80 β^- Neptunium Np-229 4.00 α 2.560 7.01 (α), 2.56 (EC), α > 50, EC < 50 Np-230 4.60 ECβ+ 3.610 3.,61 (ECβ+), 6.78 (α), ECβ+ < 97, α > 3 Np-231 48.80 ECβ+ 1.840 1.84 (EC), 6.37 (α), EC = 98, α = 2 Np-232 14.70 0.25 ECβ+ 2.700 Np-233 36.20 0.60 EC 1.230 Np-234 105.60 4.40 ECβ+ 1.810 Np-236m1 22.50 EC 1.000 1.00 (EC), 0.55 (β-), EC = 52, β- = 48 Np-238 50.81 2.12 β- 1.292 Np-239 56.52 2.36 β- 0.722 Np-240m1 7.40 0.12 β- 2.200 Np-240 65.00 1.08 β- 2.200 Np-241 13.90 β- 1.31 Np-242 5.50 β^- 2.7 Np242m1 2.20 β^- 2.7 Np-244 2.29 β^- Plutonium Pu-231 8.60 ECβ+, α Pu-232 34.10 ECβ+ 1.06 1.06 (ECβ+), 6.716 (α), EC = 77, α = 23 Pu-233 20.90 0.35 ECβ+ 1.900 Pu-234 8.80 EC 0.388 0.388 (ECβ+), 6.31 (α), EC ≈ 94, α ≈ 6 Pu-235 25.30 0.42 ECβ+ 1.170 Pu-237 45.30 EC 0.220 Pu-243 4.96 β- 0.528 Pu-245 10.50 β- 1.205 Pu-246 10.85 β- 0.401 Pu-247 2.27 β^- Americium Am-234 2.32 EC ≈ 100, α = 0.039, ECSF = 0.0066 Am-235 15.00 Am-237 73.00 1.22 EC 1.730 Am-238 98.00 1.63 EC 2.260 Am-239 11.90 EC 0.803 Am-240 50.80 2.12 EC 1.379 Am-242 16.02 β- 0.665 0.665 (β-), 0.751 (EC), β- = 82.7, EC = 17.3 Am-244m1 26.00 0.43 β- 1.516 Am-244 10.10 β- 1.428 Am-245 2.05 β- 0.894 Am-246m1 25.00 0.42 β- 2.376 Am-246 39.00 0.65 β- 2.376 Am-247 23.00 β^- 1.7 Am-248 β^- 3.1 Curium Cm-236 10.00 ECβ+ 1.710 Cm-237 20.00 Cm-238 2.40 EC 0.970 0.97 (EC), 6.62 (α), EC = 96.16, α = 3.84 Cm-239 2.90 EC 1.700 Cm-240 27.00 α 6.397 Cm-241 32.80 EC 0.767 Cm-242 162.80 α 6.216 Cm-249 64.15 1.07 β- Cm-251 16.80 β^- 1.42 Cm-252 2 β^- Berkelium Bk-240 4.80 ECβ+ 3.94 Bk-242 7.00 0.12 ECβ+ 3.000 Bk-243 4.50 EC 1.508 Bk-244 4.35 EC 2.260 Bk-245 118.56 4.94 EC 0.810 Bk-246 43.92 1.83 EC 1.350 1.35 (EC), 6.07 (α), EC = 100, α < 0,2 Bk-248m1 23.7 β- 0.870 β- = 70, EC = 30, α < 0.001, 0,87 (β-), 0.717 (EC), 5.803 (α) Bk-249 320.00 β- 0.125 Bk-250 3.22 β- 1.780 Bk-251 55.60 β- 1.093 β^- ≈ 100, α ≈ 1·10^-5 Californium Cf-241 3.78 EC 3.300 EC ≈ 75, α ≈ 25, 3.3 (EC), 7.66 (α) Cf-242 3.49 α 7.516 α = 65, SF < 1,4·10^-2 Cf-243 10.70 EC 2.220 EC ≈ 86, α ≈ 14, 2.22 (EC), 7.39 (α) Cf-244 19.40 0.32 α 7.329 Cf-245 45.00 0.75 EC 1.569 EC = 64, α = 36, 1.569 (EC), 7.256 (α) Cf-246 35.70 1.49 α 6.862 α ≈ 100, SF = 2,3·10-4, EC < 5·10-4 Cf-247 3.11 EC 0.646 EC ≈ 100, α = 0.035 Cf-248 333.50 α 6.361 Cf-253 17.81 β- 0.285 Cf-254 60.50 SF 5.926 Cf-255 85.00 β- 0.700 Cf-256 12.30 α 5.600 SF = 100, β^- < 1, α ≈ 1·10^-6 Einsteinium Es-246 7.70 EC 3.880 EC = 90.1, α = 9,9, ECSF = 0.003 Es-247 4.55 EC 2.480 2.48 (EC), 7.49 (α), EC ≈ 93, α ≈ 7 Es-248 27.00 0.45 EC Es-249 102.00 1.70 EC 1.450 Es-250 8.60 EC 2.100 Es-250m1 132.00 2.2 EC 2.100 2.10 (EC), 6.88 (α), EC ≈ 100, α < 1 Es-251 33.00 1.38 EC 0.376 Es-253 20.47 α 6.739 Es-254m1 39.30 1.64 α, β- Es-254 275.70 α 6.618 Es-255 39.80 β- 0.288 Es-256 25.40 β- 1.67 Es-256m1 456.00 7.6 β- 1.67 β^- ≈ 100, SF = 0.002 Es-257 7.8 Fermium FM-249 2.60 EC 2.440 EC ≈ 85, α ≈ 15, 2.44 (EC), 7.81 (α) Fm-250 30.00 0.50 α 7.557 7.557 (α), 0.8 (EC), α> 90, EC < 10, SF = 0.0069 Fm-251 5.30 EC 1.474 1.474 (EC), 7.425 (α), EC = 98.20, α = 1.80 Fm-252 22.70 α 7.425 Fm-253 72.00 3.00 EC 0.333 0.333 (EC), 7.197 (α), EC = 88, α = 12 Fm-254 3.24 α 7.307 α ≈ 100, SF = 0.0592 Fm-255 20.07 α 7.241 Fm-256 157.60 2.60 α 7.027 SF = 91.9, α = 8.1 Fm-257 100.50 α 6.864 Mendelevium Md-251 4.00 EC 3.070 3,07 (EC), 8,02 (α), EC > 90, α < 10 Md-252 2.30 EC 3.89 EC > 50, α < 50 Md-253 6.00 ECβ+ 1.96 Md-254 10.00 EC 2.68 EC < 100 Md-254m1 28.00 EC EC < 100 Md-255 27.00 EC 1.043 1.043 (EC), 7.907 (α), EC = 92, α = 8, SF < 1.4 Md-256 78.10 EC 2.130 2.13 (EC), 7.897 (α), EC = 90.7, α = 9.3, SF < 2.8 Md-257 5.52 EC 0.406 0.406 (EC), 7.271 (α), EC = 85, α = 15, SF < 1 Md-258 51.50 α 7.241 7.271 (α), 1.23 (EC), α ≈ 100, SF < 0.003, β- < 0.003, EC < 0.003 Md-258m1 57.00 EC 1.230 EC > 70, SF < 30, α < 1.2, β- < 30 Md-259 96.00 1.60 α 7.100 SF > 73, α < 25, β- < 10, 7.0 (α), 1.0 (β-) Md-260 27.80 α 7.000 SF > 73, α < 25, β^- < 10 Nobelium No-255 3.10 α 8.445 α = 61.4, EC = 38.w6 No-259 58.00 α 7.910 α ≈ 100, EC = 25, SF < 10 Lawrencium Lr-261 39.00 SF SF < 100 Lr-262 216.00 EC 2.1 EC> 10, SF < 10 Rutherfordium Rf-263 15.00 SF Seaborgium Sg-271 2.40 α, SF α > 50, SF < 50 Hassium Hs-278 11.00 SF Meitnerium Mt-278 30.00 α 9.1 Roentgenium Rg-282 4.00 α, SF 9.4 Nithonium Nh-285 2.00 α, SF 10 Nh-286 5.00 α 9.7 Nh-287 20.00 α, SF 9.3