PITAVASTATIN CALCIUM PENTAHYDRATE

Details

Stereochemistry	ABSOLUTE
Molecular Formula	2C25H23FNO4.Ca.5H2O
Molecular Weight	971.06
Optical Activity	UNSPECIFIED
Defined Stereocenters	4 / 4
E/Z Centers	2
Charge	0

SHOW SMILES / InChI

Structure of PITAVASTATIN CALCIUM PENTAHYDRATE

Structure Search

SMILES

O.O.O.O.O.[Ca++].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.O[C@H](C[C@H](O)\C=C\C5=C(C6=CC=C(F)C=C6)C7=CC=CC=C7N=C5C8CC8)CC([O-])=O

InChI

InChIKey=NDBJDUMINXAFLN-VKBJLXQDSA-L

InChI=1S/2C25H24FNO4.Ca.5H2O/c2*26-17-9-7-15(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;;;;;;/h2*1-4,7-12,16,18-19,28-29H,5-6,13-14H2,(H,30,31);;5*1H2/q;;+2;;;;;/p-2/b2*12-11+;;;;;;/t2*18-,19-;;;;;;/m11....../s1

HIDE SMILES / InChI

Molecular Formula	C25H23FNO4
Molecular Weight	420.4528
Charge	-1
Count

Stereochemistry	ABSOLUTE
Additional Stereochemistry	No
Defined Stereocenters	2 / 2
E/Z Centers	1
Optical Activity	UNSPECIFIED

Molecular Formula	H2O
Molecular Weight	18.0153
Charge	0
Count

Stereochemistry	ACHIRAL
Additional Stereochemistry	No
Defined Stereocenters	0 / 0
E/Z Centers	0
Optical Activity	NONE

Molecular Formula	Ca
Molecular Weight	40.078
Charge	2
Count

Stereochemistry	ACHIRAL
Additional Stereochemistry	No
Defined Stereocenters	0 / 0
E/Z Centers	0
Optical Activity	NONE

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 49 Target ID: CHEMBL402 Sources: https://www.ncbi.nlm.nih.gov/pubmed/20699675	Inhibitor 8504		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 8583	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 8583	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
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
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

AUC

Value	Dose	Co-administered	Analyte	Population
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
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

T_1/2

Value	Dose	Co-administered	Analyte	Population
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
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

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	unhealthy, adult Health Status: unhealthy Age Group: adult Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf	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
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	unhealthy, adult Health Status: unhealthy Age Group: adult Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf	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
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	unhealthy, adult Health Status: unhealthy Age Group: adult Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf	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
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	unhealthy, adult Health Status: unhealthy Age Group: adult Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf	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
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	unhealthy, adult Health Status: unhealthy Age Group: adult Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf	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
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	unhealthy, adult Health Status: unhealthy Age Group: adult Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf	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
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	unhealthy, adult Health Status: unhealthy Age Group: adult Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_MedR_P1.pdf	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

AEs

Overview

CYP3A4	CYP2C9	CYP2D6	hERG
substrate 1946 inhibitor 2252	substrate 1193 inhibitor 2438	substrate 1388 inhibitor 2507

OverviewOther

Other Inhibitor	Other Substrate	Other Inducer
CYP2C8 1057 CYP1A1 132 CYP1A2 2153 CYP1B1 32 CYP2A6 879 CYP2B6 926 CYP2C19 2057 CYP2E1 1060 P-gp 1741 BCRP 910	UGT1A3 470 UGT2B7 456 CYP1B1 104 CYP2C19 1119 CYP2B6 776 CYP1A2 1197 CYP1A1 389 OATP1B1 503 OATP1B3 435 P-gp 2052 MRP2 252 BCRP 697 NTCP 22 OAT3 391 OATP1A2 67 OATP2B1 122	P-gp 301

Drug as perpetrator

Target	Modality	Activity
CYP1A1 272	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP1A2 2333	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP1B1 93	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2A6 911	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2B6 1160	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C19 2141	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C9 2497	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2D6 2546	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2E1 1146	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP3A4 2633	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
P-gp 1932	inducer 1966 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
P-gp 1932	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
BCRP 985	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/15955871/	yes [Ki 2.92 uM]
CYP2C8 1117	inhibitor 4027 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 2052	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	inconclusive
MRP2 252	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
BCRP 697	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes
CYP1A1 389	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes	pitavastatin lactone 5
CYP1A2 1197	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes	pitavastatin lactone 5
CYP1B1 104	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes
CYP2B6 776	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes	pitavastatin lactone 5
CYP2C19 1119	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes	pitavastatin lactone 5
CYP2C9 1193	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes
CYP2D6 1388	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes	pitavastatin lactone 5
CYP3A4 1946	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes	pitavastatin lactone 5
NTCP 22	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/16259759/	yes
OAT3 391	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/16259759/	yes
OATP1A2 67	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/16259759/	yes
OATP1B1 503	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes
OATP1B3 435	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes
OATP2B1 122	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/16595711/	yes
UGT1A3 470	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/208379Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes
UGT2B7 456	substrate 4014 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
eMolecules	32452448	https://www.emolecules.com/cgi-bin/more?vid=32452448
ZINC	ZINC000001534965	http://zinc15.docking.org/substances/ZINC000001534965

PubMed

Title	Date	PubMed
Early identification of clinically relevant drug interactions with the human bile salt export pump (BSEP/ABCB11).	2013-12	24014644
Detection of statin cytotoxicity is increased in cells expressing the OATP1B1 transporter.	2013-07	23564645
ATP-dependent transport of statins by human and rat MRP2/Mrp2.	2013-06-01	23562342
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.	2012-07	22472908
Pharmacokinetic interaction between pitavastatin and valsartan: a randomized, open-labeled crossover study in healthy male Korean volunteers.	2012-04	22410289
Regulation mechanism of ABCA1 expression by statins in hepatocytes.	2011-07-15	21554872
Functional characterization of mouse organic anion transporting peptide 1a4 in the uptake and efflux of drugs across the blood-brain barrier.	2010-01	19833843
Co-administration of ezetimibe enhances proteinuria-lowering effects of pitavastatin in chronic kidney disease patients partly via a cholesterol-independent manner.	2010-01	19666118
Synthesis and HMG-CoA reductase inhibition of 2-cyclopropyl-4-thiophenyl-quinoline mevalonolactones.	2009-12-01	19879766
Effects of statins on adipose tissue inflammation: their inhibitory effect on MyD88-independent IRF3/IFN-beta pathway in macrophages.	2008-05	18323514
Modulation of celecoxib- and streptozotocin-induced experimental dementia of Alzheimer's disease by pitavastatin and donepezil.	2008-03	18208924
Involvement of BCRP (ABCG2) in the biliary excretion of pitavastatin.	2005-09	15955871
Bile salt export pump (BSEP/ABCB11) can transport a nonbile acid substrate, pravastatin.	2005-08	15901796
Effect of pitavastatin on transactivation of human serum paraoxonase 1 gene.	2005-02	15690306
Contribution of vascular NAD(P)H oxidase to endothelial dysfunction in heart failure and the therapeutic effects of HMG-CoA reductase inhibitor.	2004-11	15502390
Fibrate and statin synergistically increase the transcriptional activities of PPARalpha/RXRalpha and decrease the transactivation of NFkappaB.	2002-01-11	11779144

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.

Substance Class	Chemical Created by `admin` on `Tue Apr 01 19:53:04 GMT 2025` Edited by `admin` on `Tue Apr 01 19:53:04 GMT 2025`
Record UNII	GMK323785E
Record Status	`Validated (UNII)`
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Name

Type

Language

PITAVASTATIN CALCIUM PENTAHYDRATE

Common Name

English

PITAVASTATIN CALCIUM HYDRATE

Preferred Name

English

6-HEPTENOIC ACID, 7-(2-CYCLOPROPYL-4-(4-FLUOROPHENYL)-3-QUINOLINYL)-3,5-DIHYDROXY-, CALCIUM SALT, (3R,5S,6E)-, HYDRATE (2:1:5)

Systematic Name

English

Pitavastatin calcium pentahydrate [WHO-DD]

Common Name

English

PITAVASTATIN CALCIUM HYDRATE [JAN]

Common Name

English

Code System Code Type Description

PUBCHEM

122706735