Page last updated: 2024-12-07
hepsulfam
Description
Research Excerpts
Clinical Trials
Roles
Classes
Pathways
Study Profile
Bioassays
Related Drugs
Related Conditions
Protein Interactions
Research Growth
Description
hepsulfam: structure given in first source [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]
Cross-References
| ID Source | ID |
|---|---|
| PubMed CID | 100606 |
| CHEMBL ID | 182440 |
| SCHEMBL ID | 5409150 |
| MeSH ID | M0148973 |
Synonyms (31)
| Synonym |
|---|
| NCI60_002882 |
| hepsulfam |
| 1,7-heptanediol disulfamate |
| nsc-329680 |
| 96892-57-8 |
| sulfamic acid,7-heptanediyl ester |
| nsc329680 |
| sulfamic acid, 1,7-heptanediyl ester |
| 7-sulfamoyloxyheptyl sulfamate |
| sulfamic acid 7-sulfamoyloxy-heptyl ester |
| nsc 329680 |
| sulfamic acid 1,7-heptanediyl ester |
| bdbm50154471 |
| CHEMBL182440 , |
| unii-971du2gq51 |
| 971du2gq51 , |
| SCHEMBL5409150 |
| DTXSID90242619 |
| nci-329680 |
| sulfamic acid, s,s'-1,7-heptanediyl ester |
| 1,7-heptanediyl sulfamate |
| HY-U00095 |
| CS-7131 |
| 1,7-heptanediol bissulfamate |
| nci 329680;zinc01574758 |
| heptane-1,7-diyl bis(sulfamate) |
| zinc01574758 |
| nci 329680 |
| MS-24144 |
| 7-(sulfamoyloxy)heptyl sulfamate |
| AKOS040741833 |
Research Excerpts
Overview
Hepsulfam is a bisulfamic ester which is similar in structure to busulfan. It is believed to act as a bifunctional alkylator inducing both DNA-DNA and DNA-protein crosslinks.
| Excerpt | Reference | Relevance |
|---|---|---|
| "Hepsulfam is a bisulfamic ester which is similar in structure to busulfan and is believed to act as a bifunctional alkylator inducing both DNA-DNA and DNA-protein crosslinks. " | ( Encephalopathy is the dose-limiting toxicity of intravenous hepsulfam: results of a phase I trial in patients with advanced hematological malignancies. Geller, RB; Grochow, LB; Janisch, L; Larson, RA; Milton, J; Ratain, MJ, 1995) | 1.98 |
Effects
| Excerpt | Reference | Relevance |
|---|---|---|
| "Hepsulfam has shown broad antineoplastic activity in preclinical studies." | ( A phase I clinical and pharmacokinetic trial of hepsulfam. Brown, TD; Havlin, KA; Koeller, JM; Kuhn, JG; Marshall, MV; Ravdin, PM; Rodriguez, G; Von Hoff, DD, 1991) | 1.26 |
Toxicity
| Excerpt | Reference | Relevance |
|---|---|---|
| " Human BFU-e were greatly inhibited by PZDH, whereas murine BFU-e were relatively resistant to its toxic effects." | ( Comparative toxicity of fostriecin, hepsulfam and pyrazine diazohydroxide to human and murine hematopoietic progenitor cells in vitro. Du, DL; Grieshaber, CK; Murphy, MJ; Volpe, DA, 1991) | 0.56 |
| " We have recently shown that hepsulfam was more toxic to L1210 leukemia cells than was busulfan." | ( Mechanisms of toxicity of hepsulfam in human tumor cell lines. Cook, C; Gibson, NW; Hincks, JR; Pacheco, DY, 1990) | 0.87 |
| " Several patients treated at 640 mg/m2 had clinical evidence of toxic deliriums and slowing of alpha rhythm waves on electroencephalograms indicative of a gray-matter encephalopathy." | ( Encephalopathy is the dose-limiting toxicity of intravenous hepsulfam: results of a phase I trial in patients with advanced hematological malignancies. Geller, RB; Grochow, LB; Janisch, L; Larson, RA; Milton, J; Ratain, MJ, 1995) | 0.53 |
Pharmacokinetics
| Excerpt | Reference | Relevance |
|---|---|---|
| " Pharmacokinetic studies revealed that the clearance rate of hepsulfam is linear over the dose range studied and that its plasma disposition is biphasic with mean alpha and beta half-lives of 19 +/- 18 (SE) min and 337 +/- 248 (SE) min, respectively." | ( Phase I and pharmacokinetic study of hepsulfam (NSC 329680). Donehower, RC; Ettinger, DS; Forastiere, AA; Grochow, LB; Hendricks, CB; Lubejko, B; McGuire, WP; Rowinsky, EK; Sartorius, S, 1991) | 0.8 |
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]
Protein Targets (4)
Inhibition Measurements
| Protein | Taxonomy | Measurement | Average | Min (ref.) | Avg (ref.) | Max (ref.) | Bioassay(s) |
|---|---|---|---|---|---|---|---|
| Carbonic anhydrase 1 | Homo sapiens (human) | Ki | 0.1450 | 0.0000 | 1.3726 | 10.0000 | AID238620 |
| Carbonic anhydrase 2 | Homo sapiens (human) | Ki | 0.0080 | 0.0000 | 0.7236 | 9.9200 | AID238635 |
| Cytochrome P450 2D6 | Homo sapiens (human) | IC50 (µMol) | 699.0000 | 0.0000 | 2.0151 | 10.0000 | AID240619 |
| Carbonic anhydrase 9 | Homo sapiens (human) | Ki | 0.0101 | 0.0001 | 0.7874 | 9.9000 | AID239048 |
| [prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023] | |||||||
Biological Processes (31)
Molecular Functions (15)
Ceullar Components (14)
Bioassays (24)
| Assay ID | Title | Year | Journal | Article |
|---|---|---|---|---|
| AID238620 | Inhibitory activity against cytosolic human carbonic anhydrase I | 2005 | Bioorganic & medicinal chemistry letters, Feb-01, Volume: 15, Issue:3 | Carbonic anhydrase inhibitors: synthesis and inhibition of cytosolic/tumor-associated carbonic anhydrase isozymes I, II, and IX with bis-sulfamates. |
| AID1079934 | Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source] | |||
| AID1079944 | Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source] | |||
| AID1079941 | Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source] | |||
| AID1079936 | Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source] | |||
| AID1079946 | Presence of at least one case with successful reintroduction. [column 'REINT' in source] | |||
| AID1079949 | Proposed mechanism(s) of liver damage. [column 'MEC' in source] | |||
| AID1079940 | Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source] | |||
| AID1079931 | Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source] | |||
| AID1079943 | Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source] | |||
| AID240619 | Inhibitory concentration against cytochrome P450 2D6 | 2004 | Journal of medicinal chemistry, Oct-21, Volume: 47, Issue:22 | Validation of model of cytochrome P450 2D6: an in silico tool for predicting metabolism and inhibition. |
| AID243098 | Ratio of inhibitory activity of human cytosolic carbonic anhydrase II to tumor associated carbonic anhydrase IX | 2005 | Bioorganic & medicinal chemistry letters, Feb-01, Volume: 15, Issue:3 | Carbonic anhydrase inhibitors: synthesis and inhibition of cytosolic/tumor-associated carbonic anhydrase isozymes I, II, and IX with bis-sulfamates. |
| AID1079935 | Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source] | |||
| AID1079932 | Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source] | |||
| AID1079947 | Comments (NB not yet translated). [column 'COMMENTAIRES' in source] | |||
| AID1079939 | Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source] | |||
| AID1079942 | Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source] | |||
| AID1079948 | Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source] | |||
| AID1079938 | Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source] | |||
| AID239048 | Inhibitory activity against membrane bound tumor associated human carbonic anhydrase IX | 2005 | Bioorganic & medicinal chemistry letters, Feb-01, Volume: 15, Issue:3 | Carbonic anhydrase inhibitors: synthesis and inhibition of cytosolic/tumor-associated carbonic anhydrase isozymes I, II, and IX with bis-sulfamates. |
| AID238635 | Inhibitory activity against cytosolic human carbonic anhydrase II | 2005 | Bioorganic & medicinal chemistry letters, Feb-01, Volume: 15, Issue:3 | Carbonic anhydrase inhibitors: synthesis and inhibition of cytosolic/tumor-associated carbonic anhydrase isozymes I, II, and IX with bis-sulfamates. |
| AID1079933 | Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is | |||
| AID1079945 | Animal toxicity known. [column 'TOXIC' in source] | |||
| AID1079937 | Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source] | |||
| [information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023] | ||||
Research
Studies (22)
| Timeframe | Studies, This Drug (%) | All Drugs % |
|---|---|---|
| pre-1990 | 4 (18.18) | 18.7374 |
| 1990's | 15 (68.18) | 18.2507 |
| 2000's | 2 (9.09) | 29.6817 |
| 2010's | 1 (4.55) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| [information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023] | ||
Study Types
| Publication Type | This drug (%) | All Drugs (%) |
|---|---|---|
| Trials | 3 (13.04%) | 5.53% |
| Reviews | 0 (0.00%) | 6.00% |
| Case Studies | 0 (0.00%) | 4.05% |
| Observational | 0 (0.00%) | 0.25% |
| Other | 20 (86.96%) | 84.16% |
| [information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023] | ||