General
Preferred name
COLCHICINE
Synonyms
Colchineos ()
Colchisol ()
Colcin ()
Collagen, Type II, substrate for collagenase ()
Colchicine (NSC 757) ()
Xylan ()
Colchineos, Colchisol, Colcin,NSC 757 ()
Colchicine-d6 ()
(-)-colchicine ()
Gloperba ()
Mitigare ()
Colchcine ()
Colchicinum ()
Lodoco ()
Colcrys ()
NSC-757 ()
P&D ID
PD002408
CAS
30512-31-3
64-86-8
9014-63-5
1217651-73-4
Tags
natural product
drug
nuisance
available
Approved by
FDA
First approval
1961
Drug indication
Acute gouty arthritis
Suppressant (gout)
Drug Status
approved
Max Phase
4.0
Probe control
Probe control not defined
Orthogonal probes
0
No orthogonal probes found
Similar probes
0
No structurally similar probes found
Structure
P&D probe-likeness score
Structure formats
[[ format ]]
[[ compound[format === 'MOL' ? 'molblock' : format.toLowerCase()] ]]
Description
(extracted from source data)
DESCPRITION
A major alkaloid from Colchicum autumnale L. and found also in other Colchicum species. Its primary therapeutic use is in the treatment of gout, but it has been used also in the therapy of familial Mediterranean fever (PERIODIC DISEASE).
DESCRIPTION
Colchicine is a microtubule inhibitor. It is a methoxylated analogue of (colchicein).
SARS-CoV-2 and COVID-19: There are a number of clinical trials looking at the efficacy of colchicine as a therapy to help treat, and/or prevent the development of, severe symptoms in COVID-19 patients . It has been included in an arm of the UK's RECOVERY trial. Click here to see al clochicine studies on ClinicalTrials.gov . Colchicine is predicted to target inflammation and systemic clotting abnormalities that accompany COVID-19 . This repositioning of colchicine is based both on the drug's established anti-inflammatory action, on its ability to inhibit NLRP3 inflammasome activation, and on experimental evidence that colchicine-induced neutrophil depletion inhibits the release of the endogenous antimicrobial peptide α-defensin-1 (DEFα-1; DEFA1) and reduces thrombus formation in experimental models . Background: contact factors (such as kallikrein and FXIIa) connect inflammation to the activation of coagulation, via promoting the production of DEFα-1 by activated neutrophils. DEFα-1 has pro-thrombotic activity, acting to both stabilise fibrin and thrombus formation and impeding clot resolution by reducing fibrinolysis .
In early 2021, preliminary data from the Phase 3 ColCORONA study (NCT04322682) provided some evidence that colchicine reduced hospitalisation (by 25%), progression to mechanical ventilation (by 50%) or death (by 44%) in >4100 confirmed COVID-19 patients, compared to placebo. The drug was given in an outpatient setting. A medRxiv preprint providing more details from the ColCORONA study was posted on 27th January 2021 (DOI: 10.1101/2021.01.26.21250494v1) prior to the peer review process being completed. In contrast a preprint of results from the colchicine arm of the RECOVERY trial (11340 hospitalised COVID-19 patients) reported no clinical benefit compared to standard care by any of the primary or secondary outcome measures (Horby et al., 2021; medRxiv https://doi.org/10.1101/2021.05.18.21257267). (GtoPdb)
SARS-CoV-2 and COVID-19: There are a number of clinical trials looking at the efficacy of colchicine as a therapy to help treat, and/or prevent the development of, severe symptoms in COVID-19 patients . It has been included in an arm of the UK's RECOVERY trial. Click here to see al clochicine studies on ClinicalTrials.gov . Colchicine is predicted to target inflammation and systemic clotting abnormalities that accompany COVID-19 . This repositioning of colchicine is based both on the drug's established anti-inflammatory action, on its ability to inhibit NLRP3 inflammasome activation, and on experimental evidence that colchicine-induced neutrophil depletion inhibits the release of the endogenous antimicrobial peptide α-defensin-1 (DEFα-1; DEFA1) and reduces thrombus formation in experimental models . Background: contact factors (such as kallikrein and FXIIa) connect inflammation to the activation of coagulation, via promoting the production of DEFα-1 by activated neutrophils. DEFα-1 has pro-thrombotic activity, acting to both stabilise fibrin and thrombus formation and impeding clot resolution by reducing fibrinolysis .
In early 2021, preliminary data from the Phase 3 ColCORONA study (NCT04322682) provided some evidence that colchicine reduced hospitalisation (by 25%), progression to mechanical ventilation (by 50%) or death (by 44%) in >4100 confirmed COVID-19 patients, compared to placebo. The drug was given in an outpatient setting. A medRxiv preprint providing more details from the ColCORONA study was posted on 27th January 2021 (DOI: 10.1101/2021.01.26.21250494v1) prior to the peer review process being completed. In contrast a preprint of results from the colchicine arm of the RECOVERY trial (11340 hospitalised COVID-19 patients) reported no clinical benefit compared to standard care by any of the primary or secondary outcome measures (Horby et al., 2021; medRxiv https://doi.org/10.1101/2021.05.18.21257267). (GtoPdb)
DESCRIPTION
Prevents tubulin polymerization
(LOPAC library)
[[ p.pathway_name ]]
[[ compound.targets[tid].gene_name ]]
Cell lines
145
Organisms
7
Compound Sets
35
AdooQ Bioactive Compound Library
Axon Medchem Screening Library
ChEMBL Approved Drugs
ChEMBL Drugs
Concise Guide to Pharmacology 2017/18
Concise Guide to Pharmacology 2019/20
Concise Guide to Pharmacology 2021/22
Concise Guide to Pharmacology 2023/24
CZ-OPENSCREEN Bioactive Library
Drug Repurposing Hub
DrugBank
DrugBank Approved Drugs
DrugCentral
DrugCentral Approved Drugs
DrugMAP
DrugMAP Approved Drugs
EU-OPENSCREEN Bioactive Compound Library
Guide to Pharmacology
JUMP-Target 1 Compound Set
LOPAC library
LSP-MoA library (Laboratory of Systems Pharmacology)
Mcule NIBR MoA Box Subset
MedChem Express Bioactive Compound Library
NCATS Inxight Approved Drugs
NIH Mechanistic Set
Novartis Chemogenetic Library (NIBR MoA Box)
NPC Screening Collection
Nuisance compounds in cellular assays
Prestwick Chemical Library
Reference compounds for characterizing cellular injury in high-content cellular morphology assays
ReFrame library
Selleckchem Bioactive Compound Library
TargetMol Bioactive Compound Library
The Spectrum Collection
[[ a.name ]]
[[ ligand_id ]]
free of charge
External IDs
52
Molecular Weight
399.17
Hydrogen Bond Acceptors
6
Hydrogen Bond Donors
1
Rotatable Bonds
5
Ring Count
3
Aromatic Ring Count
2
cLogP
2.87
TPSA
83.09
Fraction CSP3
0.36
Chiral centers
1.0
Largest ring
7.0
QED
0.83
Structural alerts
1
Tubulin modulation
Nuisance compounds in cellular assays
Related compounds
Custom attributes
(extracted from source data)
Selectivity
Tubulin
Pathway
Cytoskeletal Signaling
Apoptosis
Autophagy
Cell Cycle/DNA Damage
cytoskeleton
Immunology/Inflammation
Target
Microtubule
GLRA1, GLRA2, TUBA1A, TUBA1B, TUBA1C, TUBA3C, TUBA3D, TUBA3E, TUBA4A, TUBB, TUBB1, TUBB2A, TUBB2B, TUBB3, TUBB4A, TUBB4B, TUBB6, TUBB8
Tubulin inhibitor
TUBB3
Microtubule/Tubulin
NOD-like Receptor (NLR)
MOA
Microtubule Associated
Tubulin Polymerase Inhibitors
microtubule inhibitor
Member status
member
Indication
gout, fever
Disease Area
rheumatology, endocrinology
Cellular injury category
Cytoskeletal
Therapeutic Class
Gout Suppressants
Source data
