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Identification
Name Colchicine
Accession Number DB01394
Type small molecule
Groups approved
Description

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). [PubChem]
Structure Thumb
Download: MOL | SDF | SMILES | InChI
Display: 2D Structure | 3D Structure
Synonyms
Colchicin
Colchicina
Colchicinum
Salts Not Available
Brand names
Name Company
Colcrys
Brand mixtures
Brand Name Ingredients
Arnix Gel Colchicine + Hahnemann's Causticum + Ivy + Ledum Palustre + Poison Ivy + Propolis + Rhododendron Chrysanthemum + Thuja Occidentalis
Arnix HP Apis Mellifica + Bryonia + Colchicine + Hahnemann's Causticum + Ivy + Ledum Palustre + Poison Ivy + Pulsatilla + Rhododendron Chrysanthemum
Art HP Apis Mellifica + Bryonia + Colchicine + Hahnemann's Causticum + Ivy + Ledum Palustre + Poison Ivy + Pulsatilla + Rhododendron Chrysanthemum
ColBenemid Colchicine + Probenecid
DB HP Colchicine + Eugenia Jambolana + Lactic Acid + Lycopodium Clavatum + Phosphoric Acid + Phosphorus + Uranium Nitrate
Edemnix HP Apis Mellifica + Cinchona Officinalis + Colchicine + Ledum Palustre + Lycopodium Clavatum + Poison Ivy + Sambucus Nigra + Strophanthus Hispidus
Edma HP Apis Mellifica + Cinchona Officinalis + Colchicine + Ledum Palustre + Lycopodium Clavatum + Poison Ivy + Sambucus Nigra + Strophanthus Hispidus
Jnt-Nix HP Bryonia + Colchicine + Kalmia Latifolia + Ledum Palustre + Lycopodium Clavatum + Poison Ivy + Rhododendron Chrysanthemum
Sciat HP Aconitinum + Arnica Montana + Colchicine + Esculin + Hypericum Perforatum + Magnesium Phosphate Dibasic + Plumbum Metallicum + Poison Ivy
Sciatinix HP Aconitinum + Arnica Montana + Colchicine + Esculin + Hypericum Perforatum + Magnesium Phosphate Dibasic + Plumbum Metallicum + Poison Ivy
Sucurnix HP Colchicine + Eugenia Jambolana + Lactic Acid + Lycopodium Clavatum + Phosphoric Acid + Phosphorus + Uranium Nitrate
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Categories
  • Gout Suppressants
  • Tubulin Modulators
CAS number 64-86-8
Weight Average: 399.437
Monoisotopic: 399.168187537
Chemical Formula C22H25NO6
InChI Key InChIKey=IAKHMKGGTNLKSZ-UHFFFAOYSA-N
InChI
InChI=1S/C22H25NO6/c1-12(24)23-16-8-6-13-10-19(27-3)21(28-4)22(29-5)20(13)14-7-9-18(26-2)17(25)11-15(14)16/h7,9-11,16H,6,8H2,1-5H3,(H,23,24)
Plain Text
IUPAC Name
N-{3,4,5,14-tetramethoxy-13-oxotricyclo[9.5.0.0^{2,7}]hexadeca-1(16),2(7),3,5,11,14-hexaen-10-yl}acetamide
SMILES
COC1=CC2=C(C(OC)=C1OC)C1=CC=C(OC)C(=O)C=C1C(CC2)NC(C)=O
Plain Text
Mass Spec show (2.96 KB)
Taxonomy
Kingdom Not Available
Classes Not Available
Substructures Not Available
Pharmacology
Indication For treatment and relief of pain in attacks of acute gouty arthritis.
Pharmacodynamics Colchicine is a highly poisonous alkaloid, originally extracted from plants of the genus Colchicum (Autumn crocus, also known as the "Meadow saffron"). Originally used to treat rheumatic complaints and especially gout, it was also prescribed for its cathartic and emetic effects. Its present medicinal use is mainly in the treatment of gout; as well, it is being investigated for its potential use as an anti-cancer drug. It can also be used as initial treatment for pericarditis and preventing recurrences of the condition.
Mechanism of action The precise mechanism of action has not been completely established. In patients with gout, colchicine apparently interrupts the cycle of monosodium urate crystal deposition in joint tissues and the resultant inflammatory response that initiates and sustains an acute attack. Colchicine decreases leukocyte chemotaxis and phagocytosis and inhibits the formation and release of a chemotactic glycoprotein that is produced during phagocytosis of urate crystals. Colchicine also inhibits urate crystal deposition, which is enhanced by a low pH in the tissues, probably by inhibiting oxidation of glucose and subsequent lactic acid production in leukocytes. Colchicine has no analgesic or antihyperuricemic activity. Colchicine inhibits microtubule assembly in various cells, including leukocytes, probably by binding to and interfering with polymerization of the microtubule subunit tubulin. Although some studies have found that this action probably does not contribute significantly to colchicine's antigout action, a recent in vitro study has shown that it may be at least partially involved.
Absorption Colchicine is rapidly absorbed after oral administration, probably from the jejunum and ileum. However, the rate and extent of absorption are variable, depending on the tablet dissolution rate; variability in gastric emptying, intestinal motility, and pH at the absorption site; and the extent to which colchicine is bound to microtubules in gastrointestinal mucosal cells.
Volume of distribution
  • 5 to 8 L/kg [healthy young volunteers]
Protein binding Low to moderate (30 to 50%).
Metabolism Probably hepatic. Although colchicine metabolites have not been identified in humans, metabolism by mammalian hepatic microsomes has been demonstrated in vitro.
Route of elimination In healthy volunteers (n=12) 40 – 65% of 1 mg orally administered colchicine was recovered unchanged in urine. Enterohepatic recirculation and biliary excretion are also postulated to play a role in colchicine elimination.
Half life Elimination half-life is approximately 1 hour in healthy subjects, although a study with an extended sampling time reported mean terminal elimination half-life values of approximately 9 to 10.5 hours. Other studies have reported half-life values of approximately 2 hours in patients with alcoholic cirrhosis and approximately 2.5 hours in patients with familial Mediterranean fever.
Clearance
  • 0.17 L/hr/kg [familial Mediterranean fever patients with end-stage renal disease]
  • 0.73 L/hr/kg [familial Mediterranean fever patients with normal renal function]
Toxicity The onset of toxic effects is usually delayed for several hours or more after the ingestion of an acute overdose. Nausea, vomiting, abdominal pain, and diarrhea occur first. The diarrhea may be bloody due to hemorrhagic gastroenteritis. Burning sensations of the throat, stomach, and skin may be prominent symptoms. Extensive vascular damage may result in shock. Kidney damage, evidenced by hematuria and oliguria, may occur. Muscular weakness may be marked, and ascending paralysis of the central nervous system may develop; the patient usually remains conscious. Delirium and convulsions may occur. Death due to respiratory arrest may result. Although death from the ingestion of as little as 7 mg has been reported, much larger doses have been survived .
Affected organisms
  • Humans and other mammals
Pathways Not Available
Pharmacoeconomics
Manufacturers
  • Ar holding co inc
Packagers
Dosage forms
Form Route Strength
Solution / drops Oral
Solution / drops Oral
Tablet Oral
Tablet Oral
Prices
Unit description Cost Unit
Colchicine powder 306.6 USD g
Colcrys 0.6 mg tablet 5.82 USD tablet
Colchicine 0.6 mg tablet 0.58 USD tablet
Colchicine 1 mg Tablet 0.55 USD tablet
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
Patents
Country Patent Number Approved Expires (estimated)
United States 7601758 2009-02-10 2029-02-10
United States 7619004 2008-12-03 2028-12-03
Properties
State solid
Experimental Properties
Property Value Source
melting point 156 °C PhysProp
water solubility 4.5E+004 mg/L (at 25 °C) SEIDELL,A (1941)
logP 1.30 HANSCH,C ET AL. (1995)
pKa 1.85 SANGSTER (1994)
Predicted Properties
Property Value Source
water solubility 2.76e-02 g/l ALOGPS
logP 1.59 ALOGPS
logP 1.46 ChemAxon
logS -4.2 ALOGPS
pKa (strongest acidic) 15.06 ChemAxon
pKa (strongest basic) -0.038 ChemAxon
physiological charge 0 ChemAxon
hydrogen acceptor count 6 ChemAxon
hydrogen donor count 1 ChemAxon
polar surface area 83.09 ChemAxon
rotatable bond count 5 ChemAxon
refractivity 111.38 ChemAxon
polarizability 42.41 ChemAxon
References
Synthesis Reference Not Available
General Reference Not Available
External Links
Resource Link
KEGG Drug D00570 Link_out
KEGG Compound C07592 Link_out
ChEBI 23359 Link_out
ChEMBL 23359 Link_out
Therapeutic Targets Database DAP001254 Link_out
PharmGKB PA449092 Link_out
IUPHAR 2367 Link_out
Guide to Pharmacology 2367 Link_out
HET LOC Link_out
Drug Product Database 396 Link_out
RxList http://www.rxlist.com/cgi/generic/colch.htm Link_out
Drugs.com http://www.drugs.com/cdi/colchicine.html Link_out
Wikipedia http://en.wikipedia.org/wiki/Colchicine Link_out
ATC Codes
  • M04AC01
AHFS Codes
  • 92:00.00
  • 92:02.00*
PDB Entries Not Available
FDA label Not Available
MSDS show (74.9 KB)
Interactions
Drug Interactions
Drug Interaction
Atorvastatin Increased risk of rhadbomyolysis with this combination.
Bicalutamide CYP3A4 Inhibitors like bicalutamide may increase the serum concentration of colchicine. Increase monitoring for colchicine-related toxicity when using such combinations. Use extra caution in patients with impaired renal and/or hepatic function.
Cerivastatin Increased risk of rhabdomyolysis with this combination
Clarithromycin Severe colchicine toxicity can occur
Clotrimazole CYP3A4 Inhibitors (Moderate) such as clotrimazole may increase the serum concentration of colchicine. Reduce colchicine dose (for gout flares: to 1.2 mg x 1 dose, with next dose no sooner than 3 days later; for Familial Mediterranean Fever: to no more than 1.2 mg/day) when using in combination with a moderate CYP3A4 inhibitor such as erythromycin or verapamil. Increase monitoring for colchicine-related toxicity when using such combinations. Use extra caution in patients with impaired renal and/or hepatic function.
Conivaptan CYP3A4 Inhibitors (Strong) may increase the serum concentration of Colchicine. In patients with normal renal and hepatic function, reduce colchicine dose (for gout flares: to 0.6 mg x 1 dose, followed by 0.3 mg 1 hour later, with next dose no sooner than 3 days later; for gout flare prophylaxis: if target dose would otherwise be 0.6 mg daily, change to 0.3 mg every other day, and if target dose would otherwise be 0.6 mg twice daily, change to 0.3 mg daily; for Familial Mediterranean Fever: to no more than 0.6 mg/day) when using in combination with a strong CYP3A4 inhibitor such as clarithromycin or ritonavir. Increase monitoring for colchicine-related toxicity when using such combinations. Colchicine use is contraindicated in patients with impaired renal and/or hepatic function who are also receiving a strong CYP3A4 inhibitor.
Cyclosporine Increased toxicity of both drugs
Erythromycin Severe colchicine toxicity can occur
Fluvastatin Increased risk of rhabdomyolysis with this combination
Lovastatin Increased risk of rhabdomyolysis with this combination
Pitavastatin Increased incidence of adverse drug reactions (ie. rhabdomyolysis) of both colchicine and pitavastatin via pharmacodynamic synergism.
Pravastatin Increased risk of rhabdomyolysis with this combination
Rosuvastatin Increased risk of rhabdomyolysis with this combination
Simvastatin Increased risk of rhabdomyolysis with this combination
Telithromycin Telithromycin may reduce clearance of Colchicine. Consider alternate therapy or monitor for changes in the therapeutic/adverse effects of Colchicine if Telithromycin is initiated, discontinued or dose changed.
Troleandomycin Severe colchicine toxicity can occur
Verapamil Verapamil may increase the serum concentration of Colchicine. This likely occurs via Verapamil-mediated inhibition of CYP3A4 and p-glycoprotein-mediated transport. Monitor for changes in the therapeutic/adverse effects of Colchicine if Verapamil is initiated, discontinued or dose changed.
Voriconazole Voriconazole, a strong CYP3A4 inhibitor, may increase the serum concentration of colchicine by decreasing its metabolism. A dose reduction of colchicine is recommended along with increased monitoring for colchicine toxicity. Concomitant therapy is contraindicated in patients with renal and/or hepatic impairment.
Food Interactions
  • Avoid alcohol since it increases uric acid levels.
  • Drink liberally.
  • Take without regard to meals.
Targets

1. Tubulin beta-1 chain

Pharmacological action: yes
Actions: inhibitor

Tubulin is the major constituent of microtubules. It binds two moles of GTP, one at an exchangeable site on the beta chain and one at a non-exchangeable site on the alpha-chain

Organism class: human
UniProt ID: Q9H4B7 Link_out
Gene: TUBB1 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Overington JP, Al-Lazikani B, Hopkins AL: How many drug targets are there? Nat Rev Drug Discov. 2006 Dec;5(12):993-6. Pubmed
  2. Imming P, Sinning C, Meyer A: Drugs, their targets and the nature and number of drug targets. Nat Rev Drug Discov. 2006 Oct;5(10):821-34. Pubmed
  3. Acharya BR, Choudhury D, Das A, Chakrabarti G: Vitamin K3 disrupts the microtubule networks by binding to tubulin: a novel mechanism of its antiproliferative activity. Biochemistry. 2009 Jul 28;48(29):6963-74. Pubmed
  4. Li CM, Lu Y, Ahn S, Narayanan R, Miller DD, Dalton JT: Competitive mass spectrometry binding assay for characterization of three binding sites of tubulin. J Mass Spectrom. 2010 Sep 1. Pubmed
  5. Finkelstein Y, Aks SE, Hutson JR, Juurlink DN, Nguyen P, Dubnov-Raz G, Pollak U, Koren G, Bentur Y: Colchicine poisoning: the dark side of an ancient drug. Clin Toxicol (Phila). 2010 Jun;48(5):407-14. Pubmed
  6. Cerquaglia C, Diaco M, Nucera G, La Regina M, Montalto M, Manna R: Pharmacological and clinical basis of treatment of Familial Mediterranean Fever (FMF) with colchicine or analogues: an update. Curr Drug Targets Inflamm Allergy. 2005 Feb;4(1):117-24. Pubmed

2. Tubulin beta chain

Pharmacological action: yes
Actions: inhibitor

Tubulin is the major constituent of microtubules. It binds two moles of GTP, one at an exchangeable site on the beta chain and one at a non-exchangeable site on the alpha-chain

Organism class: human
UniProt ID: P07437 Link_out
Gene: TUBB Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Yee KW, Hagey A, Verstovsek S, Cortes J, Garcia-Manero G, O’Brien SM, Faderl S, Thomas D, Wierda W, Kornblau S, Ferrajoli A, Albitar M, McKeegan E, Grimm DR, Mueller T, Holley-Shanks RR, Sahelijo L, Gordon GB, Kantarjian HM, Giles FJ: Phase 1 study of ABT-751, a novel microtubule inhibitor, in patients with refractory hematologic malignancies. Clin Cancer Res. 2005 Sep 15;11(18):6615-24. Pubmed
  2. Acharya BR, Choudhury D, Das A, Chakrabarti G: Vitamin K3 disrupts the microtubule networks by binding to tubulin: a novel mechanism of its antiproliferative activity. Biochemistry. 2009 Jul 28;48(29):6963-74. Pubmed
  3. Li CM, Lu Y, Ahn S, Narayanan R, Miller DD, Dalton JT: Competitive mass spectrometry binding assay for characterization of three binding sites of tubulin. J Mass Spectrom. 2010 Sep 1. Pubmed
  4. Cerquaglia C, Diaco M, Nucera G, La Regina M, Montalto M, Manna R: Pharmacological and clinical basis of treatment of Familial Mediterranean Fever (FMF) with colchicine or analogues: an update. Curr Drug Targets Inflamm Allergy. 2005 Feb;4(1):117-24. Pubmed
Enzymes

1. Cytochrome P450 3A4

Actions: substrate, inhibitor, inducer

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It performs a variety of oxidation reactions (e.g. caffeine 8-oxidation, omeprazole sulphoxidation, midazolam 1'-hydroxylation and midazolam 4- hydroxylation) of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics. The enzyme also hydroxylates etoposide

UniProt ID: P08684 Link_out
Gene: CYP3A4
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

2. Cytochrome P450 2B6

Actions: inhibitor

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics

UniProt ID: P20813 Link_out
Gene: CYP2B6 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

3. Cytochrome P450 2C8

Actions: inhibitor, inducer

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics. In the epoxidation of arachidonic acid it generates only 14,15- and 11,12-cis-epoxyeicosatrienoic acids. It is the principal enzyme responsible for the metabolism the anti- cancer drug paclitaxel (taxol)

UniProt ID: P10632 Link_out
Gene: CYP2C8
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

4. Cytochrome P450 2C9

Actions: inhibitor, inducer

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics. This enzyme contributes to the wide pharmacokinetics variability of the metabolism of drugs such as S- warfarin, diclofenac, phenytoin, tolbutamide and losartan

UniProt ID: P11712 Link_out
Gene: CYP2C9
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

5. Cytochrome P450 2E1

Actions: inducer

Metabolizes several precarcinogens, drugs, and solvents to reactive metabolites. Inactivates a number of drugs and xenobiotics and also bioactivates many xenobiotic substrates to their hepatotoxic or carcinogenic forms

UniProt ID: P05181 Link_out
Gene: CYP2E1 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed
Transporters

1. Multidrug resistance protein 3

Actions: inducer

Mediates ATP-dependent export of organic anions and drugs from the cytoplasm. Hydrolyzes ATP with low efficiency. Human MDR3 is not capable of conferring drug resistance. Mediates the translocation of phosphatidylcholine across the canalicular membrane of the hepatocyte

UniProt ID: P21439 Link_out
Gene: ABCB4 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Vollrath V, Wielandt AM, Acuna C, Duarte I, Andrade L, Chianale J: Effect of colchicine and heat shock on multidrug resistance gene and P-glycoprotein expression in rat liver. J Hepatol. 1994 Nov;21(5):754-63. Pubmed

2. Solute carrier family 22 member 3

Actions: inhibitor

Mediates potential-dependent transport of a variety of organic cations. May play a significant role in the disposition of cationic neurotoxins and neurotransmitters in the brain

UniProt ID: O75751 Link_out
Gene: SLC22A3 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Grundemann D, Schechinger B, Rappold GA, Schomig E: Molecular identification of the corticosterone-sensitive extraneuronal catecholamine transporter. Nat Neurosci. 1998 Sep;1(5):349-51. Pubmed

3. Multidrug resistance protein 1

Actions: substrate, inhibitor

Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells

UniProt ID: P08183 Link_out
Gene: ABCB1 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Polli JW, Wring SA, Humphreys JE, Huang L, Morgan JB, Webster LO, Serabjit-Singh CS: Rational use of in vitro P-glycoprotein assays in drug discovery. J Pharmacol Exp Ther. 2001 Nov;299(2):620-8. Pubmed
  2. Schwab D, Fischer H, Tabatabaei A, Poli S, Huwyler J: Comparison of in vitro P-glycoprotein screening assays: recommendations for their use in drug discovery. J Med Chem. 2003 Apr 24;46(9):1716-25. Pubmed
  3. Nagy H, Goda K, Fenyvesi F, Bacso Z, Szilasi M, Kappelmayer J, Lustyik G, Cianfriglia M, Szabo G Jr: Distinct groups of multidrug resistance modulating agents are distinguished by competition of P-glycoprotein-specific antibodies. Biochem Biophys Res Commun. 2004 Mar 19;315(4):942-9. Pubmed
  4. Troutman MD, Thakker DR: Novel experimental parameters to quantify the modulation of absorptive and secretory transport of compounds by P-glycoprotein in cell culture models of intestinal epithelium. Pharm Res. 2003 Aug;20(8):1210-24. Pubmed
  5. Ambudkar SV, Lelong IH, Zhang J, Cardarelli CO, Gottesman MM, Pastan I: Partial purification and reconstitution of the human multidrug-resistance pump: characterization of the drug-stimulatable ATP hydrolysis. Proc Natl Acad Sci U S A. 1992 Sep 15;89(18):8472-6. Pubmed
  6. Bebawy M, Morris MB, Roufogalis BD: A continuous fluorescence assay for the study of P-glycoprotein-mediated drug efflux using inside-out membrane vesicles. Anal Biochem. 1999 Mar 15;268(2):270-7. Pubmed
  7. Kuo CC, Hsieh HP, Pan WY, Chen CP, Liou JP, Lee SJ, Chang YL, Chen LT, Chen CT, Chang JY: BPR0L075, a novel synthetic indole compound with antimitotic activity in human cancer cells, exerts effective antitumoral activity in vivo. Cancer Res. 2004 Jul 1;64(13):4621-8. Pubmed
  8. Tiwari AK, Sodani K, Wang SR, Kuang YH, Ashby CR Jr, Chen X, Chen ZS: Nilotinib (AMN107, Tasigna) reverses multidrug resistance by inhibiting the activity of the ABCB1/Pgp and ABCG2/BCRP/MXR transporters. Biochem Pharmacol. 2009 Jul 15;78(2):153-61. Epub 2009 Apr 11. Pubmed

4. Multidrug resistance-associated protein 1

Actions: substrate

May participate directly in the active transport of drugs into subcellular organelles or influence drug distribution indirectly. Confers resistance to anticancer drugs. Transports LTC4. May protect milk against xenobiotics

UniProt ID: P33527 Link_out
Gene: ABCC1 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Stride BD, Grant CE, Loe DW, Hipfner DR, Cole SP, Deeley RG: Pharmacological characterization of the murine and human orthologs of multidrug-resistance protein in transfected human embryonic kidney cells. Mol Pharmacol. 1997 Sep;52(3):344-53. Pubmed
Comments
Drug created on July 08, 2007 11:02 / Updated on February 08, 2013 16:20