PITAVASTATIN

Details

Stereochemistry	ABSOLUTE
Molecular Formula	C25H24FNO4
Molecular Weight	421.4608
Optical Activity	UNSPECIFIED
Defined Stereocenters	2 / 2
E/Z Centers	1
Charge	0

SHOW SMILES / InChI

Structure Search

SMILES

O[C@H](C[C@H](O)\C=C\C1=C(C2=CC=C(F)C=C2)C3=CC=CC=C3N=C1C4CC4)CC(O)=O

InChI

InChIKey=VGYFMXBACGZSIL-MCBHFWOFSA-N

InChI=1S/C25H24FNO4/c26-17-9-7-15(8-10-17)24-20-3-1-2-4-22(20)27-25(16-5-6-16)21(24)12-11-18(28)13-19(29)14-23(30)31/h1-4,7-12,16,18-19,28-29H,5-6,13-14H2,(H,30,31)/b12-11+/t18-,19-/m1/s1

HIDE SMILES / InChI

Description
Sources: http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/022363s012lbl.pdf
Curator's Comment: description was created based on several sources, including https://www.ncbi.nlm.nih.gov/pubmed/20179258

Pitavastatin is a new synthetic 3-hydroxy-3-methyl glutaryl coenzyme A reductase (HMG-CoA reductase) inhibitor, which was developed, and has been available in Japan since July 2003. Metabolism of pitavastatin by the cytochrome P450 (CYP) system is minimal, principally through CYP 2C9, with little involvement of the CYP 3A4 isoenzyme, potentially reducing the risk of drug-drug interactions between pitavastatin and other drugs known to inhibit CYP enzymes. To date, human and animal studies have shown pitavastatin to be potentially as effective in lowering LDL-cholesterol levels as rosuvastatin. Pitavastatin under the trade name Livalo is indicated as an adjunctive therapy to diet to reduce elevated total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (Apo B), triglycerides (TG), and to increase HDL-C in adult patients with primary hyperlipidemia or mixed dyslipidemia. Pitavastatin competitively inhibits HMG-CoA reductase, which is a rate-determining enzyme involved with biosynthesis of cholesterol, in a manner of competition with the substrate so that it inhibits cholesterol synthesis in the liver. As a result, the expression of LDL-receptors followed by the uptake of LDL from blood to liver is accelerated and then the plasma TC decreases. Further, the sustained inhibition of cholesterol synthesis in the liver decreases levels of very low density lipoproteins. Common statin-related side effects (headaches, stomach upset, abnormal liver function tests and muscle cramps) were similar to other statins.

CNS Activity

Originator

Approval Year

Targets

Primary Target	Pharmacology	Condition	Potency
HMG-CoA reductase 47 Target ID: CHEMBL402 Sources: https://www.ncbi.nlm.nih.gov/pubmed/20699675	Inhibitor 8297		1.7 nM [Ki]

Conditions

Condition	Modality	Targets	Highest Phase	Product
Primary hyperlipidemia 7 Sources: http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/022363s012lbl.pdf	Primary		Approved 8429	LIVALO Approved Use Drug therapy should be one component of multiple-risk-factor intervention in individuals who require modifications of their lipid profile. Lipid-altering agents should be used in addition to a diet restricted in saturated fat and cholesterol only when the response to diet and other nonpharmacological measures has been inadequate. LIVALO is a HMG-CoA reductase inhibitor indicated for: Patients with primary hyperlipidemia or mixed dyslipidemia as an adjunctive therapy to diet to reduce elevated total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (Apo B), triglycerides (TG), and to increase high-density lipoprotein cholesterol (HDL-C) (1.1) Limitations of Use (1.2): Doses of LIVALO greater than 4 mg once daily were associated with an increased risk for severe myopathy in premarketing clinical studies. Do not exceed 4 mg once daily dosing of LIVALO. The effect of LIVALO on cardiovascular morbidity and mortality has not been determined. LIVALO has not been studied in Fredrickson Type I, III, and V dyslipidemias. 1.1 Primary Hyperlipidemia and Mixed Dyslipidemia LIVALO® is indicated as an adjunctive therapy to diet to reduce elevated total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (Apo B), triglycerides (TG), and to increase HDL-C in adult patients with primary hyperlipidemia or mixed dyslipidemia. 1.2 Limitations of Use Doses of LIVALO greater than 4 mg once daily were associated with an increased risk for severe myopathy in premarketing clinical studies. Do not exceed 4 mg once daily dosing of LIVALO. The effect of LIVALO on cardiovascular morbidity and mortality has not been determined. LIVALO has not been studied in Fredrickson Type I, III, and V dyslipidemias. Launch Date 2009
Mixed dyslipidemia 8 Sources: http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/022363s012lbl.pdf	Primary		Approved 8429	LIVALO Approved Use Drug therapy should be one component of multiple-risk-factor intervention in individuals who require modifications of their lipid profile. Lipid-altering agents should be used in addition to a diet restricted in saturated fat and cholesterol only when the response to diet and other nonpharmacological measures has been inadequate. LIVALO is a HMG-CoA reductase inhibitor indicated for: Patients with primary hyperlipidemia or mixed dyslipidemia as an adjunctive therapy to diet to reduce elevated total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (Apo B), triglycerides (TG), and to increase high-density lipoprotein cholesterol (HDL-C) (1.1) Limitations of Use (1.2): Doses of LIVALO greater than 4 mg once daily were associated with an increased risk for severe myopathy in premarketing clinical studies. Do not exceed 4 mg once daily dosing of LIVALO. The effect of LIVALO on cardiovascular morbidity and mortality has not been determined. LIVALO has not been studied in Fredrickson Type I, III, and V dyslipidemias. 1.1 Primary Hyperlipidemia and Mixed Dyslipidemia LIVALO® is indicated as an adjunctive therapy to diet to reduce elevated total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (Apo B), triglycerides (TG), and to increase HDL-C in adult patients with primary hyperlipidemia or mixed dyslipidemia. 1.2 Limitations of Use Doses of LIVALO greater than 4 mg once daily were associated with an increased risk for severe myopathy in premarketing clinical studies. Do not exceed 4 mg once daily dosing of LIVALO. The effect of LIVALO on cardiovascular morbidity and mortality has not been determined. LIVALO has not been studied in Fredrickson Type I, III, and V dyslipidemias. Launch Date 2009

C_max

Value	Dose	Co-administered	Analyte	Population
98.4 ng/mL EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/26082816	2 mg single, oral dose: 2 mg route of administration: Oral experiment type: SINGLE co-administered:		PITAVASTATIN blood	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FASTED
113 ng/mL EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/26082816	2 mg single, oral dose: 2 mg route of administration: Oral experiment type: SINGLE co-administered:		PITAVASTATIN blood	Homo sapiens population: HEALTHY age: ADULT sex: FEMALE food status: FASTED

AUC

Value	Dose	Co-administered	Analyte	Population
285.77 ng × h/mL EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/26082816	2 mg single, oral dose: 2 mg route of administration: Oral experiment type: SINGLE co-administered:		PITAVASTATIN blood	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FASTED
329.96 ng × h/mL EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/26082816	2 mg single, oral dose: 2 mg route of administration: Oral experiment type: SINGLE co-administered:		PITAVASTATIN blood	Homo sapiens population: HEALTHY age: ADULT sex: FEMALE food status: FASTED

T_1/2

Value	Dose	Co-administered	Analyte	Population
9.08 h EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/26082816	2 mg single, oral dose: 2 mg route of administration: Oral experiment type: SINGLE co-administered:		PITAVASTATIN blood	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FASTED
9.95 h EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/26082816	2 mg single, oral dose: 2 mg route of administration: Oral experiment type: SINGLE co-administered:		PITAVASTATIN blood	Homo sapiens population: HEALTHY age: ADULT sex: FEMALE food status: FASTED

Doses

Dose	Population	Adverse events
64 mg 1 times / day steady, oral Highest studied dose Dose: 64 mg, 1 times / day Route: oral Route: steady Dose: 64 mg, 1 times / day Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87	unhealthy, adult n = 33 Health Status: unhealthy Condition: primary hyperlipidemia or mixed dyslipidemia Age Group: adult Population Size: 33 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87	Disc. AE: Gastrointestinal disorders, Fatigue... AEs leading to discontinuation/dose reduction: Gastrointestinal disorders (3%) Fatigue (9.1%) ALT increased (9.1%) AST increased (9.1%) Aspartate aminotransferase abnormal NOS (6.1%) CPK increased (12.1%) Blood creatine phosphokinase abnormal (6.1%) Myalgia (18.2%) Myopathy (6.1%) Pain in extremity (3%) Rhabdomyolysis (9.1%) Renal and urinary disorders (6.1%) Proteinuria (3%) Renal failure (3%) Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87
1 mg 1 times / day steady, oral Recommended Dose: 1 mg, 1 times / day Route: oral Route: steady Dose: 1 mg, 1 times / day Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87	unhealthy, adult n = 309 Health Status: unhealthy Condition: primary hyperlipidemia or mixed dyslipidemia Age Group: adult Population Size: 309 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87	Disc. AE: Fatigue... AEs leading to discontinuation/dose reduction: Fatigue (0.3%) Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87
2 mg 1 times / day steady, oral Recommended Dose: 2 mg, 1 times / day Route: oral Route: steady Dose: 2 mg, 1 times / day Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87	unhealthy, adult n = 951 Health Status: unhealthy Condition: primary hyperlipidemia or mixed dyslipidemia Age Group: adult Population Size: 951 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87	Disc. AE: Fatigue, ALT increased... AEs leading to discontinuation/dose reduction: Fatigue (0.3%) ALT increased (0.1%) Myalgia (0.7%) Urinary retention (0.1%) Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87
4 mg 1 times / day steady, oral Recommended Dose: 4 mg, 1 times / day Route: oral Route: steady Dose: 4 mg, 1 times / day Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87	unhealthy, adult n = 1540 Health Status: unhealthy Condition: primary hyperlipidemia or mixed dyslipidemia Age Group: adult Population Size: 1540 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87	Disc. AE: Fatigue, CPK increased... AEs leading to discontinuation/dose reduction: Fatigue (0.1%) CPK increased (0.1%) Pollakiuria (0.1%) Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87
16 mg 1 times / day steady, oral Dose: 16 mg, 1 times / day Route: oral Route: steady Dose: 16 mg, 1 times / day Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87	unhealthy, adult n = 102 Health Status: unhealthy Condition: primary hyperlipidemia or mixed dyslipidemia Age Group: adult Population Size: 102 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87	Disc. AE: Fatigue, Pyrexia... AEs leading to discontinuation/dose reduction: Fatigue (2.9%) Pyrexia (2%) CPK increased (10.8%) ALT increased (5.9%) AST increased (4.9%) Back pain (2%) Myalgia (5.9%) Myopathy (1%) Rhabdomyolysis (1%) Myoglobinuria (1%) Proteinuria (1%) Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87
32 mg 1 times / day steady, oral Dose: 32 mg, 1 times / day Route: oral Route: steady Dose: 32 mg, 1 times / day Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87	unhealthy, adult n = 34 Health Status: unhealthy Condition: primary hyperlipidemia or mixed dyslipidemia Age Group: adult Population Size: 34 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87	Disc. AE: Gastrointestinal disorders, ALT increased... AEs leading to discontinuation/dose reduction: Gastrointestinal disorders (2.9%) ALT increased (11.8%) AST increased (11.8%) Blood creatine phosphokinase abnormal (2.9%) CPK increased (5.9%) Myalgia (8.8%) Rhabdomyolysis (5.9%) Myoglobinuria (2.9%) Renal and urinary disorders (2.9%) Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87
8 mg 1 times / day steady, oral Dose: 8 mg, 1 times / day Route: oral Route: steady Dose: 8 mg, 1 times / day Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87	unhealthy, adult n = 479 Health Status: unhealthy Condition: primary hyperlipidemia or mixed dyslipidemia Age Group: adult Population Size: 479 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87	Disc. AE: Fatigue, CPK increased... AEs leading to discontinuation/dose reduction: Fatigue (0.2%) CPK increased (0.4%) Rhabdomyolysis (0.4%) Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf Page: p. 87

AEs

Overview

CYP3A4	CYP2C9	CYP2D6	hERG
substrate 1737 inhibitor 1587	substrate 1037 inhibitor 1767	substrate 1217 inhibitor 1852

OverviewOther

Other Inhibitor	Other Substrate	Other Inducer
CYP2C8 911 CYP1A1 110 CYP1A2 1524 CYP1B1 19 CYP2A6 707 CYP2B6 810 CYP2C19 1478 CYP2E1 882 P-gp 1461 BCRP 699	UGT1A3 422 UGT2B7 389 CYP1B1 92 CYP2C19 991 CYP2B6 664 CYP1A2 1054 CYP1A1 349 OATP1B1 406 OATP1B3 350 P-gp 1537 MRP2 205 BCRP 561 NTCP 17 OAT3 339 OATP1A2 62 OATP2B1 104	P-gp 257

Drug as perpetrator

Target	Modality	Activity
CYP1A1 218	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP1A2 1692	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP1B1 67	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2A6 739	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2B6 1001	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C19 1553	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C9 1819	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2D6 1891	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2E1 970	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP3A4 1925	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
P-gp 1650	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
P-gp 1650	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
BCRP 773	inhibitor 3277 Sources: https://pubmed.ncbi.nlm.nih.gov/15955871/	yes [Ki 2.92 uM]
CYP2C8 965	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes

Drug as victim

Target	Modality	Activity	Metabolite
P-gp 1537	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	inconclusive
MRP2 205	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
BCRP 561	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes
CYP1A1 349	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes	pitavastatin lactone 5
CYP1A2 1054	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes	pitavastatin lactone 5
CYP1B1 92	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes
CYP2B6 664	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes	pitavastatin lactone 5
CYP2C19 991	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes	pitavastatin lactone 5
CYP2C9 1037	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes
CYP2D6 1217	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes	pitavastatin lactone 5
CYP3A4 1737	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes	pitavastatin lactone 5
NTCP 17	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/16259759/	yes
OAT3 339	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/16259759/	yes
OATP1A2 62	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/16259759/	yes
OATP1B1 406	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes
OATP1B3 350	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes
OATP2B1 104	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/16595711/	yes
UGT1A3 422	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes
UGT2B7 389	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes

Sourcing

Vendor/Aggregator	ID	URL
ChEBI	CHEBI:32020	https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:32020
ChemicalBook	CB6206668	https://www.chemicalbook.com/ChemicalProductProperty_EN_CB6206668
ZINC	ZINC000001534965	http://zinc15.docking.org/substances/ZINC000001534965
eMolecules	32452448	https://www.emolecules.com/cgi-bin/more?vid=32452448

PubMed

Title	Date	PubMed
Synthesis and HMG-CoA reductase inhibition of 2-cyclopropyl-4-thiophenyl-quinoline mevalonolactones.	2009 Dec 1	19879766
Comparison of the safety, tolerability, and pharmacokinetic profile of a single oral dose of pitavastatin 4 mg in adult subjects with severe renal impairment not on hemodialysis versus healthy adult subjects.	2012 Jul	22472908
Early identification of clinically relevant drug interactions with the human bile salt export pump (BSEP/ABCB11).	2013 Dec	24014644
Detection of statin cytotoxicity is increased in cells expressing the OATP1B1 transporter.	2013 Jul	23564645
ATP-dependent transport of statins by human and rat MRP2/Mrp2.	2013 Jun 1	23562342

Patents

Sample Use Guides

In Vivo Use Guide

1 to 4 mg orally once daily at any time of the day with or without food. The recommended starting dose is 2 mg and the maximum dose is 4 mg

Route of Administration: Oral

In Vitro Use Guide

The liver cancer cells Huh-7 and SMMC7721 were trypsinized into single cells and split into 24-well dishes at 100 cells/well. The cells were pretreated with 0 µM, 0.5 µM, or 1 µM of pitavastatin and cultured for 8 days. Pitavastatin treatment increased the population of Huh-7 cells in the sub-G1 phase. It induced apoptosis of liver cancer cells. It was found that caspase-9 and caspase-3 as well as poly ADP ribose polymerase (PARP) were cleaved.

Name

Type

Language

PITAVASTATIN

Official Name

English

PITAVASTATIN [MI]

Common Name

English

pitavastatin [INN]

Common Name

English

PITAVASTATIN [MART.]

Common Name

English

Pitavastatin [WHO-DD]

Common Name

English

NSC-760423

Code

English

(3R,5S,6E)-7-(2-CYCLOPROPYL-4-(P-FLUOROPHENYL)-3-QUINOLYL)-3,5-DIHYDROXY-6-HEPTENOIC ACID

Common Name

English

K-924 component Pivastatin

Code

English

ITAVASTATIN

Common Name

English

NIKITA

Brand Name

English

PITAVASTATIN [VANDF]

Common Name

English

Classification Tree Code System Code

WHO-VATC

QC10AA08