ID Source | ID |
---|---|
PubMed CID | 656604 |
CHEMBL ID | 80830 |
CHEBI ID | 31312 |
SCHEMBL ID | 121965 |
MeSH ID | M0087059 |
Synonym |
---|
CHEMBL80830 , |
bucilant |
(r)-3-mercapto-2-(2-mercapto-2-methylpropanamido)propanoic acid |
AKOS015841445 |
de-019 |
sa-96 |
tiobutarit |
bucillamine , |
rimatil |
n-(2-mercapto-2-methylpropionyl)-l-cysteine |
bucilamina [spanish] |
n-(2-mercapto-2-methyl-1-oxopropyl)-l-cysteine |
ccris 5260 |
sa96 |
bucillaminum [latin] |
bucillamine [inn:jan] |
n-(2-mercaptoisobutyryl)-l-cysteine |
l-cysteine, n-(2-mercapto-2-methyl-1-oxopropyl)- |
n-(2-mercapto-2-methylpropanoyl)-l-cysteine |
thiobutarit |
D01809 |
65002-17-7 |
bucilant (tn) |
bucillamine (jp17/inn) |
(2r)-2-[(2-methyl-2-sulfanylpropanoyl)amino]-3-sulfanylpropanoic acid |
(2r)-2-[(2-methyl-2-sulfanyl-propanoyl)amino]-3-sulfanyl-propanoic acid |
(2r)-3-mercapto-2-[(2-mercapto-2-methyl-1-oxopropyl)amino]propanoic acid |
A834941 |
NCGC00182062-02 |
NCGC00183271-01 |
dtxsid2048587 , |
dtxcid2028513 |
tox21_112916 |
tox21_113147 |
cas-65002-17-7 |
AM62722 |
bdbm50406934 |
r80lra5wtf , |
unii-r80lra5wtf |
bucillaminum |
bucilamina |
AKOS015895462 |
RB3025 |
bucillamine [mart.] |
bucillamine [inn] |
bucillamine [who-dd] |
bucillamine [jan] |
bucillamine [mi] |
MLS006010100 |
smr004701240 |
SCHEMBL121965 |
VUAFHZCUKUDDBC-BYPYZUCNSA-N |
Q-101254 |
AC-32465 |
mfcd00867570 |
sr-01000883966 |
SR-01000883966-1 |
CHEBI:31312 |
KS-1449 |
DB12160 |
Q4982752 |
(r)-3-mercapto-2-(2-mercapto-2-methylpropanamido)-propanoic acid |
BCP12127 |
de019; sa96;thiobutarit;rimatil. |
HY-118530 |
Bucillamine (Bc) is a cysteine derivative with two SH groups, and a homolog of D-penicillamine, a disease-modifying antirheumatic drug (DMARD) widely used in Japan. Bucillamine is a low molecular weight thiol antioxidant that is capable of rapidly entering cells.
Bucillamine has potential to attenuate or prevent damage during myocardial infarction, cardiac surgery and organ transplantation. Bucillamine found to have beneficial effects in the treatment of rheumatoid arthritis.
Excerpt | Reference | Relevance |
---|---|---|
"Bucillamine has potential to attenuate or prevent damage during myocardial infarction, cardiac surgery and organ transplantation. " | ( Bucillamine: a potent thiol donor with multiple clinical applications. Horwitz, LD, 2003) | 3.2 |
"Bucillamine (BUC) has been found to have beneficial effects in the treatment of rheumatoid arthritis (RA), in which the activation of endothelial cells plays an important role in the pathogenesis. " | ( Inhibitory effects of bucillamine on the expression of vascular cell adhesion molecule-1 in human umbilical vein endothelial cells. Hirohata, S; Isshi, K; Kikuchi, H, 2004) | 2.08 |
"Bucillamine has been reported to have beneficial effects in rheumatoid arthritis. " | ( [A case of rheumatoid arthritis associated with agranulocytosis during bucillamine treatment]. Hashimoto, M; Hiramatsu, K; Hosaka, M; Iwabuchi, H; Kaga, S; Kanemitsu, H; Kasama, T; Matsuda, A; Negishi, M; Yamazaki, J, 1994) | 1.96 |
"Bucillamine, which has two donatable thiol groups, was twice as protective as N-2-mercaptopropionyl glycine, which contains a single donatable thiol group." | ( Bucillamine prevents myocardial reperfusion injury. Horwitz, LD; Sherman, NA, 2001) | 2.47 |
Bucillamine can cause corticosteroid-resistant and life-threatening lung injury. Bucillamine could also suppress T cell binding to rIFN-gamma treated EC as well as untreated EC.
Excerpt | Reference | Relevance |
---|---|---|
"Bucillamine can cause corticosteroid-resistant and life-threatening lung injury, especially in the elderly." | ( A case with life-threatening interstitial pneumonia associated with bucillamine treatment. Makino, F; Mochizuki, H; Morioka, T; Ogiwara, Y; Sugihara, T; Takahashi, H, 2008) | 1.3 |
"Bucillamine could also suppress T cell binding to rIFN-gamma treated EC as well as untreated EC." | ( Bucillamine inhibits T cell adhesion to human endothelial cells. Eguchi, K; Fukuda, T; Ida, H; Ishimaru, T; Kawakami, A; Nakashima, M; Sakai, M; Shimada, H; Terada, K; Yamashita, I, 1992) | 2.45 |
Bucillamine (BCL), a treatment for rheumatoid arthritis, occasionally causes proteinuria. In treatment with bucillamine, therefore, the drug should be carefully administered and regular blood examinations carried out to prevent the occurrence of this side effect.
Excerpt | Reference | Relevance |
---|---|---|
"SA96 in combination with indomethacin or prednisolone was investigated for their effects on the adjuvant arthritis in Lewis rats." | ( [Pharmacological studies of N-(2-mercapto-2-methylpropanoyl)-L-cysteine (SA96). V. Effects of SA96 in combination with indomethacin or prednisolone on adjuvant arthritis in rats]. Hayashi, M; Iso, T; Kasamatsu, S; Mibu, H; Nakata, K; Yamauchi, H, 1985) | 0.27 |
Excerpt | Reference | Relevance |
---|---|---|
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs." | ( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein. Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019) | 0.51 |
Excerpt | Relevance | Reference |
---|---|---|
" BUC-ID, but not BUC, appeared to suppress the expression of VCAM-1 on HUVEC stimulated with TNF-alpha in a dose-response manner at its pharmacologically relevant concentrations (0." | ( Inhibitory effects of bucillamine on the expression of vascular cell adhesion molecule-1 in human umbilical vein endothelial cells. Hirohata, S; Isshi, K; Kikuchi, H, 2004) | 0.64 |
" Recent change in permitted maximum dosage of MTX from 8 to 16 mg/week may improve its efficacy and continuation rate in treating Japanese RA patients." | ( Recent trends in use of nonbiologic DMARDs and evaluation of their continuation rates in single and dual combination therapies in rheumatoid arthritis patients in Japan. Kageyama, M; Kempe, K; Kon, T; Kusaoi, M; Matsudaira, R; Matsushita, M; Ogasawara, M; Onuma, S; Sekiya, F; Sugimoto, K; Tada, K; Takasaki, Y; Tamura, N; Yamaji, K, 2012) | 0.38 |
Class | Description |
---|---|
organic molecular entity | Any molecular entity that contains carbon. |
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res] |
Protein | Taxonomy | Measurement | Average (µ) | Min (ref.) | Avg (ref.) | Max (ref.) | Bioassay(s) |
---|---|---|---|---|---|---|---|
estrogen nuclear receptor alpha | Homo sapiens (human) | Potency | 9.5205 | 0.0002 | 29.3054 | 16,493.5996 | AID743069 |
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023] |
Protein | Taxonomy | Measurement | Average | Min (ref.) | Avg (ref.) | Max (ref.) | Bioassay(s) |
---|---|---|---|---|---|---|---|
Angiotensin-converting enzyme | Homo sapiens (human) | IC50 (µMol) | 7,244.3599 | 0.0001 | 0.5336 | 10.0000 | AID39018 |
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023] |
Process | via Protein(s) | Taxonomy |
---|---|---|
extracellular space | Angiotensin-converting enzyme | Homo sapiens (human) |
extracellular region | Angiotensin-converting enzyme | Homo sapiens (human) |
extracellular space | Angiotensin-converting enzyme | Homo sapiens (human) |
lysosome | Angiotensin-converting enzyme | Homo sapiens (human) |
endosome | Angiotensin-converting enzyme | Homo sapiens (human) |
plasma membrane | Angiotensin-converting enzyme | Homo sapiens (human) |
external side of plasma membrane | Angiotensin-converting enzyme | Homo sapiens (human) |
basal plasma membrane | Angiotensin-converting enzyme | Homo sapiens (human) |
brush border membrane | Angiotensin-converting enzyme | Homo sapiens (human) |
extracellular exosome | Angiotensin-converting enzyme | Homo sapiens (human) |
sperm midpiece | Angiotensin-converting enzyme | Homo sapiens (human) |
plasma membrane | Angiotensin-converting enzyme | Homo sapiens (human) |
[Information is prepared from geneontology information from the June-17-2024 release] |
Assay ID | Title | Year | Journal | Article |
---|---|---|---|---|
AID1346986 | P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen | 2019 | Molecular pharmacology, 11, Volume: 96, Issue:5 | A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein. |
AID1296008 | Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening | 2020 | SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1 | Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening. |
AID651635 | Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression | |||
AID1346987 | P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen | 2019 | Molecular pharmacology, 11, Volume: 96, Issue:5 | A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein. |
AID1079940 | Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' 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] | |||
AID1079947 | Comments (NB not yet translated). [column 'COMMENTAIRES' in source] | |||
AID1079943 | Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source] | |||
AID1079934 | Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source] | |||
AID1079948 | Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source] | |||
AID1079942 | Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source] | |||
AID1079939 | Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source] | |||
AID1079949 | Proposed mechanism(s) of liver damage. [column 'MEC' in source] | |||
AID1079932 | Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source] | |||
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 | |||
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] | |||
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] | |||
AID1079944 | Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source] | |||
AID39018 | Inhibitory activity against angiotensin converting enzyme (ACE) | 1993 | Journal of medicinal chemistry, Aug-06, Volume: 36, Issue:16 | Three-dimensional quantitative structure-activity relationship of angiotesin-converting enzyme and thermolysin inhibitors. II. A comparison of CoMFA models incorporating molecular orbital fields and desolvation free energies based on active-analog and com |
AID1079945 | Animal toxicity known. [column 'TOXIC' in source] | |||
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] | |||
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] | |||
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] | |||
AID1079946 | Presence of at least one case with successful reintroduction. [column 'REINT' in source] | |||
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023] |
Timeframe | Studies, This Drug (%) | All Drugs % |
---|---|---|
pre-1990 | 15 (8.38) | 18.7374 |
1990's | 57 (31.84) | 18.2507 |
2000's | 69 (38.55) | 29.6817 |
2010's | 33 (18.44) | 24.3611 |
2020's | 5 (2.79) | 2.80 |
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023] |
According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be strong demand-to-supply ratio for research on this compound.
| This Compound (39.89) All Compounds (24.57) |
Publication Type | This drug (%) | All Drugs (%) |
---|---|---|
Trials | 11 (5.70%) | 5.53% |
Reviews | 28 (14.51%) | 6.00% |
Case Studies | 48 (24.87%) | 4.05% |
Observational | 0 (0.00%) | 0.25% |
Other | 106 (54.92%) | 84.16% |
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023] |
Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
Multi-Center, Randomized, Double-Blind, Placebo-Controlled Study of Bucillamine in Patients With Mild-Moderate COVID-19 [NCT04504734] | Phase 3 | 713 participants (Actual) | Interventional | 2020-11-27 | Terminated(stopped due to Met definition of futility according to DSMB) | ||
A Randomized, Double-blind, Multicenter Study Evaluating the Safety and Efficacy of Sarilumab Added to Non-MTX DMARDs or as Monotherapy in Japanese Patients With Active Rheumatoid Arthritis [NCT02373202] | Phase 3 | 91 participants (Actual) | Interventional | 2015-02-28 | Completed | ||
The Bucillamine Study of Holding Remission After Infliximab Dose-off in Patients With Rheumatoid Arthritis Receiving Methotrexate [NCT00716248] | Phase 4 | 40 participants (Anticipated) | Interventional | 2007-01-31 | Active, not recruiting | ||
Phase 2 Multi-Center, Dose Escalation Trial To Assess The Safety And Effectiveness Of Bucillamine On Urinary Cystine Excretion And Cystine Capacity In Patients With Cystinuria [NCT02942420] | Phase 2 | 30 participants (Anticipated) | Interventional | 2017-05-01 | Recruiting | ||
A RANDOMIZED, MULTICENTRE PHASE IIa OPEN-LABEL, ACTIVE-COMPARATOR TRIAL TO ASSESS THE EFFICACY AND SAFETY OF TWO REGIMENS OF BUCILLAMINE 100 MG TABLETS AS COMPARED TO COLCHICINE 0.6 MG TABLETS FOR THE TREATMENT OF AN ACUTE GOUT FLARE IN SUBJECTS WITH MODE [NCT02330796] | Phase 2 | 66 participants (Actual) | Interventional | 2015-04-30 | Completed | ||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |