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Identification
NamePrasugrel
Accession NumberDB06209
TypeSmall Molecule
GroupsApproved
Description

Prasugrel, a thienopyridine derivative, is a platelet activation and aggregation inhibitor structurally and pharmacologically related to clopidogrel and ticlopidine. Similar to clopidogrel, prasugrel is a prodrug that requires enzymatic transformation in the liver to its active metabolite, R-138727. R-138727 irreversibly binds to P2Y12 type ADP receptors on platelets thus preventing activation of the GPIIb/IIIa receptor complex. As a result, inhibition of ADP-mediated platelet activation and aggregation occurs. Prasugrel was developed by Daiichi Sankyo Co. and is currently marketed in the United States and Canada in cooperation with Eli Lilly and Company for acute coronary syndromes planned for percutaneous coronary intervention (PCI). FDA approved in 2009.

Structure
Thumb
Synonyms
Effient
Prasugrel
External Identifiers
  • CS-747
  • LY-640315
Approved Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
Effienttablet, film coated5 mg/1oralEli Lilly and Company2012-03-01Not applicableUs
Effienttablet, film coated10 mg/1oralCardinal Health2012-03-01Not applicableUs
Effienttablet10 mgoralEli Lilly Canada Inc2010-05-17Not applicableCanada
Effienttablet, film coated10 mg/1oralPhysicians Total Care, Inc.2011-03-15Not applicableUs
Effienttablet, film coated10 mg/1oralEli Lilly and Company2012-03-01Not applicableUs
Approved Generic Prescription ProductsNot Available
Approved Over the Counter ProductsNot Available
Unapproved/Other Products Not Available
International Brands
NameCompany
EfientDaiichi Sankyo Co.
PrasitaDaiichi Sankyo Co.
Brand mixturesNot Available
Salts
Name/CASStructureProperties
Prasugrel Hydrochloride
Thumb
  • InChI Key: JALHGCPDPSNJNY-UHFFFAOYNA-N
  • Monoisotopic Mass: 409.091470145
  • Average Mass: 409.902
DBSALT000145
Categories
UNII34K66TBT99
CAS number150322-43-3
WeightAverage: 373.441
Monoisotopic: 373.114792406
Chemical FormulaC20H20FNO3S
InChI KeyInChIKey=DTGLZDAWLRGWQN-UHFFFAOYSA-N
InChI
InChI=1S/C20H20FNO3S/c1-12(23)25-18-10-14-11-22(9-8-17(14)26-18)19(20(24)13-6-7-13)15-4-2-3-5-16(15)21/h2-5,10,13,19H,6-9,11H2,1H3
IUPAC Name
5-[2-cyclopropyl-1-(2-fluorophenyl)-2-oxoethyl]-4H,5H,6H,7H-thieno[3,2-c]pyridin-2-yl acetate
SMILES
CC(=O)OC1=CC2=C(CCN(C2)C(C(=O)C2CC2)C2=CC=CC=C2F)S1
Taxonomy
DescriptionThis compound belongs to the class of organic compounds known as phenylpropylamines. These are compounds containing a phenylpropylamine moiety, which consists of a phenyl group substituted at the third carbon by an propan-1-amine.
KingdomOrganic compounds
Super ClassBenzenoids
ClassBenzene and substituted derivatives
Sub ClassPhenylpropylamines
Direct ParentPhenylpropylamines
Alternative Parents
Substituents
  • Phenylpropylamine
  • Thienopyridine
  • 2,3,5-trisubstituted thiophene
  • Aralkylamine
  • Halobenzene
  • Fluorobenzene
  • Pyridine
  • Aryl halide
  • Aryl fluoride
  • Heteroaromatic compound
  • Acetate salt
  • Thiophene
  • Alpha-aminoketone
  • Tertiary aliphatic amine
  • Tertiary amine
  • Ketone
  • Carboxylic acid ester
  • Azacycle
  • Organoheterocyclic compound
  • Monocarboxylic acid or derivatives
  • Carboxylic acid derivative
  • Hydrocarbon derivative
  • Organooxygen compound
  • Organonitrogen compound
  • Organofluoride
  • Organohalogen compound
  • Carbonyl group
  • Amine
  • Aromatic heteropolycyclic compound
Molecular FrameworkAromatic heteropolycyclic compounds
External DescriptorsNot Available
Pharmacology
IndicationIndicated in combination with acetylsalicylic acid (ASA) to prevent atherothrombotic events in patients with acute coronary syndrome (ACS) who are to be managed with percutaneous coronary intervention (PCI). May be used in patients with unstable angina (UA), non-ST elevation myocardial infarction (NSTEMI), ST-elevation myocardial infarction (STEMI) who are to be managed with PCI. Prasugrel is not recommended in patients 75 years of age or greater, those that weigh<60kg, and patients with a history of stroke or transient ischemic attack due to increased risk of fatal and intracranial bleeding.
PharmacodynamicsPrasugrel is a member of the thienopyridine class of ADP receptor inhibitors, like ticlopidine (trade name Ticlid) and clopidogrel (trade name Plavix). These agents reduce the aggregation ("clumping") of platelets by irreversibly binding to P2Y12 receptors. Compared to clopidogrel, prasugrel inhibits adenosine diphosphate–induced platelet aggregation more rapidly, more consistently, and to a greater extent than do standard and higher doses of clopidogrel in healthy volunteers and in patients with coronary artery disease, including those undergoing PCI. The increased potency of prasugrel appears to be due to more efficient conversion to its active metabolite. However, it carries a higher risk of bleed compared to clopidogrel, which may be a result of its higher potency. Prasugrel produces inhibition of platelet aggregation to 20 μM or 5 μM ADP, as measured by light transmission aggregometry.
Mechanism of actionPrasugrel is an thienopyridine and a prodrug which inhibits ADP receptors by irreversibly acting on the P2Y12 receptor on platelets. The active metabolite of prasugrel prevents binding of adenosine diphosphate (ADP) to its platelet receptor, impairing the ADP-mediated activation of the glycoprotein GPIIb/IIIa complex. Prasugrel is proposed to have a similar mechanism of action to clopidogrel.
Related Articles
Absorption79% or greater of the dose is absorbed after oral administration. Absorption and metabolism occur rapidly and peak plasma concentrations (Cmax) are reached approximately 30 minutes following oral administration. Administration with a high fat, high calorie meal did not affect the AUC of the active metabolite in healthy individuals, but the Cmax was decreased by ~49% and the Tmax was increased to 0.5 to 1.5 hours. Prasugrel may be administered with or without food.
Volume of distribution

44-68L

Protein bindingApproximately 98% of the active metabolite was bound to human serum albumin in a 4% buffered solution. The major inactive metabolites are also highly bound to human plasma proteins.
Metabolism

Prasugrel is not detected in plasma following oral administration. It is rapidly hydrolyzed in the intestine to thiolactone by human carboxylesterase (hCE) 2. This intermediate is further metabolized to its active metabolite, R-138727, in a single step by cytochrome P450 enzymes in the liver (primarily CYP3A4 and CYP2B6 and to a lesser extent by CYP2C9 and CYP2C19). The active metabolite is further metabolized by S-methylation or cysteine conjugation to two inactive metabolites. Unlike clopidogrel, transformation of prasugrel to its active metabolite does not appear to be affected by cytochrome P450 polymorphisms.

SubstrateEnzymesProduct
Prasugrel
R-95913Details
R-95913
R-138727Details
Route of eliminationApproximately 68% of the orally administered dose is excreted in urine and 27% in the feces, as inactive metabolites. The active metabolite is not expected to be removed by dialysis.
Half lifeThe active metabolite has an elimination half-life of about 7.4 hours (range 2-15 hours).
Clearance

Apparent clearance = 112 – 166 L/hr

ToxicityLD50 (rat) 1,000 - 2,000 mg/kg; LD50 (rabbit) > 1,000 mg/kg
Affected organisms
  • Humans and other mammals
PathwaysNot Available
SNP Mediated EffectsNot Available
SNP Mediated Adverse Drug ReactionsNot Available
ADMET
Predicted ADMET features
PropertyValueProbability
Human Intestinal Absorption+1.0
Blood Brain Barrier+0.9352
Caco-2 permeable+0.5325
P-glycoprotein substrateSubstrate0.767
P-glycoprotein inhibitor IInhibitor0.6555
P-glycoprotein inhibitor IINon-inhibitor0.7365
Renal organic cation transporterInhibitor0.5312
CYP450 2C9 substrateNon-substrate0.7508
CYP450 2D6 substrateNon-substrate0.7371
CYP450 3A4 substrateSubstrate0.5402
CYP450 1A2 substrateNon-inhibitor0.5288
CYP450 2C9 inhibitorNon-inhibitor0.5706
CYP450 2D6 inhibitorNon-inhibitor0.7051
CYP450 2C19 inhibitorInhibitor0.7083
CYP450 3A4 inhibitorNon-inhibitor0.7432
CYP450 inhibitory promiscuityHigh CYP Inhibitory Promiscuity0.8719
Ames testNon AMES toxic0.6616
CarcinogenicityNon-carcinogens0.9521
BiodegradationNot ready biodegradable0.9961
Rat acute toxicity2.4834 LD50, mol/kg Not applicable
hERG inhibition (predictor I)Weak inhibitor0.7927
hERG inhibition (predictor II)Non-inhibitor0.6438
ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397 )
Pharmacoeconomics
ManufacturersNot Available
PackagersNot Available
Dosage forms
FormRouteStrength
Tabletoral10 mg
Tablet, film coatedoral10 mg/1
Tablet, film coatedoral5 mg/1
PricesNot Available
Patents
Patent NumberPediatric ExtensionApprovedExpires (estimated)
CA2077695 No2002-08-202012-09-08Canada
US5288726 No1997-04-142017-04-14Us
US6693115 No2001-07-032021-07-03Us
US8404703 No2003-01-022023-01-02Us
US8569325 No2003-01-022023-01-02Us
Properties
StateSolid
Experimental Properties
PropertyValueSource
logP3.536MSDS
Predicted Properties
PropertyValueSource
Water Solubility0.00237 mg/mLALOGPS
logP3.67ALOGPS
logP4.31ChemAxon
logS-5.2ALOGPS
pKa (Strongest Acidic)14.25ChemAxon
pKa (Strongest Basic)5.48ChemAxon
Physiological Charge0ChemAxon
Hydrogen Acceptor Count3ChemAxon
Hydrogen Donor Count0ChemAxon
Polar Surface Area46.61 Å2ChemAxon
Rotatable Bond Count6ChemAxon
Refractivity96.81 m3·mol-1ChemAxon
Polarizability37.7 Å3ChemAxon
Number of Rings4ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectra
Mass Spec (NIST)Not Available
SpectraNot Available
References
Synthesis Reference

Teruhiko Inoue, Kazuyoshi Nakamura, Masahiko Hagihara, Hiroyuki Miyata, Yukinori Wada, Naoyuki Yokota, “Process for Producing High-Purity Prasugrel and Acid Addition Salt Thereof.” U.S. Patent US20090203729, issued August 13, 2009.

US20090203729
General References
  1. Dovlatova NL, Jakubowski JA, Sugidachi A, Heptinstall S: The reversible P2Y antagonist cangrelor influences the ability of the active metabolites of clopidogrel and prasugrel to produce irreversible inhibition of platelet function. J Thromb Haemost. 2008 Jul;6(7):1153-9. doi: 10.1111/j.1538-7836.2008.03020.x. Epub 2008 Jul 1. [PubMed:18485086 ]
  2. Tagarakis GI: Ticagrelor and prasugrel: two novel, most-promising antiplatelet agents. Recent Pat Cardiovasc Drug Discov. 2010 Nov;5(3):208-11. [PubMed:20874669 ]
  3. Angiolillo DJ: The evolution of antiplatelet therapy in the treatment of acute coronary syndromes: from aspirin to the present day. Drugs. 2012 Nov 12;72(16):2087-116. doi: 10.2165/11640880-000000000-00000. [PubMed:23083110 ]
  4. Jeong YH, Tantry US, Gurbel PA: Importance of potent P2Y(12) receptor blockade in acute myocardial infarction: focus on prasugrel. Expert Opin Pharmacother. 2012 Aug;13(12):1771-96. doi: 10.1517/14656566.2012.704909. Epub 2012 Jul 12. [PubMed:22783896 ]
External Links
ATC CodesB01AC22
AHFS Codes
  • 20:12.18
PDB EntriesNot Available
FDA labelDownload (1000 KB)
MSDSDownload (134 KB)
Interactions
Drug Interactions
Drug
AbciximabPrasugrel may increase the anticoagulant activities of Abciximab.
AcenocoumarolPrasugrel may increase the anticoagulant activities of Acenocoumarol.
Acetylsalicylic acidThe risk or severity of adverse effects can be increased when Prasugrel is combined with Acetylsalicylic acid.
AlteplasePrasugrel may increase the anticoagulant activities of Alteplase.
AnistreplasePrasugrel may increase the anticoagulant activities of Anistreplase.
ApixabanThe risk or severity of adverse effects can be increased when Prasugrel is combined with Apixaban.
AtazanavirThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Atazanavir resulting in a loss in efficacy.
BoceprevirThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Boceprevir resulting in a loss in efficacy.
CangrelorCangrelor may decrease the antiplatelet activities of Prasugrel.
CeritinibThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Ceritinib resulting in a loss in efficacy.
Citric AcidPrasugrel may increase the anticoagulant activities of Citric Acid.
ClarithromycinThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Clarithromycin resulting in a loss in efficacy.
CobicistatThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Cobicistat resulting in a loss in efficacy.
CollagenaseThe risk or severity of adverse effects can be increased when Prasugrel is combined with Collagenase.
Dabigatran etexilatePrasugrel may increase the anticoagulant activities of Dabigatran etexilate.
DalteparinPrasugrel may increase the anticoagulant activities of Dalteparin.
DarunavirThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Darunavir resulting in a loss in efficacy.
DasatinibDasatinib may increase the anticoagulant activities of Prasugrel.
Deoxycholic AcidThe risk or severity of adverse effects can be increased when Prasugrel is combined with Deoxycholic Acid.
DicoumarolPrasugrel may increase the anticoagulant activities of Dicoumarol.
Edetic AcidPrasugrel may increase the anticoagulant activities of Edetic Acid.
EnoxaparinPrasugrel may increase the anticoagulant activities of Enoxaparin.
Ethyl biscoumacetatePrasugrel may increase the anticoagulant activities of Ethyl biscoumacetate.
Fondaparinux sodiumPrasugrel may increase the anticoagulant activities of Fondaparinux sodium.
GlucosamineGlucosamine may increase the antiplatelet activities of Prasugrel.
HeparinPrasugrel may increase the anticoagulant activities of Heparin.
Ibritumomab tiuxetanThe risk or severity of adverse effects can be increased when Prasugrel is combined with Ibritumomab.
IbrutinibThe risk or severity of adverse effects can be increased when Ibrutinib is combined with Prasugrel.
IdelalisibThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Idelalisib resulting in a loss in efficacy.
IndinavirThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Indinavir resulting in a loss in efficacy.
ItraconazoleThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Itraconazole resulting in a loss in efficacy.
KetoconazoleThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Ketoconazole resulting in a loss in efficacy.
LimaprostLimaprost may increase the antiplatelet activities of Prasugrel.
NefazodoneThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Nefazodone resulting in a loss in efficacy.
NelfinavirThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Nelfinavir resulting in a loss in efficacy.
ObinutuzumabThe risk or severity of adverse effects can be increased when Prasugrel is combined with Obinutuzumab.
Omega-3 fatty acidsOmega-3 fatty acids may increase the antiplatelet activities of Prasugrel.
Pentosan PolysulfateThe risk or severity of adverse effects can be increased when Pentosan Polysulfate is combined with Prasugrel.
PentoxifyllinePentoxifylline may increase the antiplatelet activities of Prasugrel.
PhenindionePrasugrel may increase the anticoagulant activities of Phenindione.
PhenprocoumonPrasugrel may increase the anticoagulant activities of Phenprocoumon.
PosaconazoleThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Posaconazole resulting in a loss in efficacy.
RanitidineThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Ranitidine resulting in a loss in efficacy.
ReteplasePrasugrel may increase the anticoagulant activities of Reteplase.
RidogrelPrasugrel may increase the anticoagulant activities of Ridogrel.
RifampicinRifampicin may decrease the antiplatelet activities of Prasugrel.
RitonavirThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Ritonavir resulting in a loss in efficacy.
RivaroxabanPrasugrel may increase the anticoagulant activities of Rivaroxaban.
SaquinavirThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Saquinavir resulting in a loss in efficacy.
StreptokinasePrasugrel may increase the anticoagulant activities of Streptokinase.
SulodexidePrasugrel may increase the anticoagulant activities of Sulodexide.
TelaprevirThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Telaprevir resulting in a loss in efficacy.
TelithromycinThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Telithromycin resulting in a loss in efficacy.
TenecteplasePrasugrel may increase the anticoagulant activities of Tenecteplase.
TipranavirTipranavir may increase the antiplatelet activities of Prasugrel.
TositumomabThe risk or severity of adverse effects can be increased when Prasugrel is combined with Tositumomab.
TreprostinilPrasugrel may increase the anticoagulant activities of Treprostinil.
UrokinasePrasugrel may increase the anticoagulant activities of Urokinase.
Vitamin EVitamin E may increase the antiplatelet activities of Prasugrel.
VoriconazoleThe serum concentration of the active metabolites of Prasugrel can be reduced when Prasugrel is used in combination with Voriconazole resulting in a loss in efficacy.
WarfarinPrasugrel may increase the anticoagulant activities of Warfarin.
Food Interactions
  • Despite being a CYP3A4 inducer, grapefruit juice does not affect the pharmacokinetics of prasugrel

Targets

Kind
Protein
Organism
Human
Pharmacological action
yes
Actions
antagonist
General Function:
Guanyl-nucleotide exchange factor activity
Specific Function:
Receptor for ADP and ATP coupled to G-proteins that inhibit the adenylyl cyclase second messenger system. Not activated by UDP and UTP. Required for normal platelet aggregation and blood coagulation.
Gene Name:
P2RY12
Uniprot ID:
Q9H244
Molecular Weight:
39438.355 Da
References
  1. Dovlatova NL, Jakubowski JA, Sugidachi A, Heptinstall S: The reversible P2Y antagonist cangrelor influences the ability of the active metabolites of clopidogrel and prasugrel to produce irreversible inhibition of platelet function. J Thromb Haemost. 2008 Jul;6(7):1153-9. doi: 10.1111/j.1538-7836.2008.03020.x. Epub 2008 Jul 1. [PubMed:18485086 ]

Enzymes

Kind
Protein
Organism
Human
Pharmacological action
unknown
Actions
substrate
General Function:
Methylumbelliferyl-acetate deacetylase activity
Specific Function:
Involved in the detoxification of xenobiotics and in the activation of ester and amide prodrugs. Shows high catalytic efficiency for hydrolysis of cocaine, 4-methylumbelliferyl acetate, heroin and 6-monoacetylmorphine.
Gene Name:
CES2
Uniprot ID:
O00748
Molecular Weight:
61806.41 Da
References
  1. Angiolillo DJ: The evolution of antiplatelet therapy in the treatment of acute coronary syndromes: from aspirin to the present day. Drugs. 2012 Nov 12;72(16):2087-116. doi: 10.2165/11640880-000000000-00000. [PubMed:23083110 ]
Kind
Protein
Organism
Human
Pharmacological action
yes
Actions
substrate
General Function:
Vitamin d3 25-hydroxylase activity
Specific Function:
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 xenobiot...
Gene Name:
CYP3A4
Uniprot ID:
P08684
Molecular Weight:
57342.67 Da
References
  1. Angiolillo DJ: The evolution of antiplatelet therapy in the treatment of acute coronary syndromes: from aspirin to the present day. Drugs. 2012 Nov 12;72(16):2087-116. doi: 10.2165/11640880-000000000-00000. [PubMed:23083110 ]
Kind
Protein
Organism
Human
Pharmacological action
yes
Actions
substrate
General Function:
Steroid hydroxylase activity
Specific Function:
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. Acts as a 1,4-cineole 2-exo-monooxygenase.
Gene Name:
CYP2B6
Uniprot ID:
P20813
Molecular Weight:
56277.81 Da
References
  1. Angiolillo DJ: The evolution of antiplatelet therapy in the treatment of acute coronary syndromes: from aspirin to the present day. Drugs. 2012 Nov 12;72(16):2087-116. doi: 10.2165/11640880-000000000-00000. [PubMed:23083110 ]
Kind
Protein
Organism
Human
Pharmacological action
yes
Actions
substrate
General Function:
Steroid hydroxylase activity
Specific Function:
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, phenyto...
Gene Name:
CYP2C9
Uniprot ID:
P11712
Molecular Weight:
55627.365 Da
References
  1. Angiolillo DJ: The evolution of antiplatelet therapy in the treatment of acute coronary syndromes: from aspirin to the present day. Drugs. 2012 Nov 12;72(16):2087-116. doi: 10.2165/11640880-000000000-00000. [PubMed:23083110 ]
Kind
Protein
Organism
Human
Pharmacological action
yes
Actions
substrate
General Function:
Steroid hydroxylase activity
Specific Function:
Responsible for the metabolism of a number of therapeutic agents such as the anticonvulsant drug S-mephenytoin, omeprazole, proguanil, certain barbiturates, diazepam, propranolol, citalopram and imipramine.
Gene Name:
CYP2C19
Uniprot ID:
P33261
Molecular Weight:
55930.545 Da
References
  1. Angiolillo DJ: The evolution of antiplatelet therapy in the treatment of acute coronary syndromes: from aspirin to the present day. Drugs. 2012 Nov 12;72(16):2087-116. doi: 10.2165/11640880-000000000-00000. [PubMed:23083110 ]

Carriers

Kind
Protein
Organism
Human
Pharmacological action
unknown
Actions
substrate
General Function:
Toxic substance binding
Specific Function:
Serum albumin, the main protein of plasma, has a good binding capacity for water, Ca(2+), Na(+), K(+), fatty acids, hormones, bilirubin and drugs. Its main function is the regulation of the colloidal osmotic pressure of blood. Major zinc transporter in plasma, typically binds about 80% of all plasma zinc.
Gene Name:
ALB
Uniprot ID:
P02768
Molecular Weight:
69365.94 Da
Comments
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Drug created on March 19, 2008 10:17 / Updated on July 27, 2016 01:57