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HuagongsheHuagongshe Chemistry Print Report · For research reference only
HCID 5282452Generated: October 27, 2026

Pitavastatin

PITVASTATIN · ITAVASTATIN · PITAVASTATIN · PitavastatinCa · Compound T7072 · D4-Pitavastatin · pitavastatin(1-) · Pitavastatin API

https://huagongshe.com/en/chemical/5282452

Pitavastatin molecular structure

Identifiers & Physical Properties

CAS No.147511-69-1
Molecular formulaC25H24FNO4
Average molar mass421.5 g/mol
Monoisotopic mass421.16893647 g/mol
SMILESO=C(O)C[C@H](O)C[C@H](O)/C=C/c1c(C2CC2)nc2ccccc2c1-c1ccc(F)cc1
InChIKeyVGYFMXBACGZSIL-MCBHFWOFSA-N
PubChem CID5282452
ChEMBLCHEMBL1201753
ChEBICHEBI:32020
EC No.643-092-3
DTXSIDDTXSID1048384

Chemical & Physical Properties

XLogP3.5
Topological polar surface area90.7
Hydrogen bond donors3
Hydrogen bond acceptors6
Rotatable bonds8
Heavy atoms31
Formal charge0
Complexity631
DrugsPharmaceuticals -> StatinsPharmaceuticals -> AntilipidemicsPharmaceuticals -> Listed in ZINC15
SolubilityVery slightly solubleChloroform (Slightly), Methanol (Slightly)
Human DrugsBreast FeedingLactationMilk, HumanAnticholesteremic AgentsHypolipidemic AgentsHydroxymethylglutaryl-CoA Reductase Inhibitors
Optical RotationMW: 881.00. White to pale-yellow, odorless powder. Lipophilic. Specific optical rotation: +23.1 deg at 20 °C/D (c = 1 in acetonitrile/water). freely soluble in pyridine, chlorform, dilute hydrochloric acid, tetrahydrofuransoluble in ethylene glycolsparingly soluble in octanolslightly soluble in methanolvery slightly soluble in water, ethanol. Practically insoluble in acetonitrile, diethyl ether. Hydgroscopicslightly unstable in light. /Pitavasatin calcium salt/
Collision Cross Section202.3 Ų [M+H]+ [CCS Type: DTBuffer gas: N2Ionization: APCI+Dataset: TOXCASTSource Identifier: DTXSID4046448]
Other Experimental PropertiesMW: 493.45. MP: 138-139 °C. Specific optical rotation: +8.84 deg at 32 °C/D (c = 0.92 in chloroform). Soluble in acetonitrile /Pitavastatin lactone/
Melting point182 - 185°C
Boiling point692.0±55.0 °C(Predicted)
Density1.352±0.06 g/cm3(Predicted)
Storage conditions-20°C, Hygroscopic
pKa (acidity coefficient)4.24±0.10(Predicted)
Physical stateSolid
ColorWhite to Off-White
StabilityHygroscopic
InChIKeyVGYFMXBACGZSIL-MCBHFWOFSA-N
SMILESC(O)(=O)C[C@H](O)C[C@H](O)/C=C/C1=C(C2=CC=C(F)C=C2)C2C(N=C1C1CC1)=CC=CC=2
CAS DataBase Reference147511-69-1(CAS DataBase Reference)
FDA UNIIM5681Q5F9P
ATC codeC10AA08
EPA Substance Registry System6-Heptenoic acid, 7-[2-cyclopropyl-4-(4-fluorophenyl)-3-quinolinyl]-3,5-dihydroxy-, (3R,5S,6E)- (147511-69-1)
GHS pictogramGHS07
Signal wordWarning
GHS hazard statementsH302-H315-H319-H335
GHS precautionary statementsP261-P305+P351+P338
Hazardous substances data147511-69-1(Hazardous Substances Data)

Safety & Regulations

GHS classificationWarningH361 (100%): Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]P203, P260, P263, P264, P270, P280, P318, P405, and P501 (click each P-code to see the statement)The GHS information provided by 1 company from 1 notification to the ECHA C&L Inventory.
FDA requirementsThe Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including pitavastatin calcium, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Pitavastatin calcium/
Hazard Classes and CategoriesRepr. 2 (100%)
Storage conditionsStore at room temperature between 15 °C and 30 °C (59 deg to 86 °F). Protect from light.
Disposal methodsSRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.
InteractionsPitavastatin is a substrate of organic anionic transport polypeptide (OATP) 1B1 (OATP2). Drugs that inhibit OATP1B1 (e.g., cyclosporine, erythromycin, rifampin) can increase bioavailability of pitavastatin.Concomitant use of pitavastatin (2 mg once daily) and ezetimibe (10 mg for 7 days) decreased pitavastatin peak plasma concentration and AUC by 2 and 0.2%, respectively, and increased ezetimibe peak plasma concentration and AUC by 9 and 2%, respectively.Erythromycin substantially increases pitavastatin exposure.1 Following concomitant use of pitavastatin (4 mg as a single dose on day 4) and erythromycin (500 mg 4 times daily for 6 days), pitavastatin peak plasma concentration and AUC were increased by 3.6- and 2.8-fold, respectivelysuch effects were considered clinically important. The interaction between pitavastatin and erythromycin probably resulted partly from erythromycin-induced inhibition of organic anionic transport polypeptide (OATP)1B1-mediated hepatic uptake of pitavastatin. If used concomitantly with erythromycin, dosage of pitavastatin should not exceed 1 mg once daily.

Applications & Uses

Description

Pitavastatin (Brand Name: LIVALO) is an inhibitor of HMG-CoA reductase which catalyzes the first step of cholesterol synthesis. It appears as odorless and white to pale-yellow powder. It takes effects by reducing the level of certain fatty substances such as cholesterol in the body. Therefore, it is mainly indicated for the treatment of hypercholesterolaemia and for the prevention of cardiovascular diseases. It can not only lower the high cholesterol and triglyceride in certain patients, but also can increase the content of high density lipoprotein (HDL), the “good” cholesterol levels. It should be generally administrated together with a proper diet.

Uses

HMGA reductase inhibitor

Concomitant use of pitavastatin (4 mg once daily on days 1-5 and 11-15) and extended-release diltiazem hydrochloride (240 mg on days 6-15) increased pitavastatin peak plasma concentration and AUC by 15 and 10%, respectively, and decreased diltiazem peak plasma concentration and AUC by 7 and 2%, respectively.
For more Interactions (Complete) data for Pitavastatin (20 total), please visit the HSDB record page.
HepatotoxicityLess information is available on the potential hepatotoxicity of pitavastatin in comparison to other more widely used statins. In large clinical trials, pitavastatin therapy was associated with mild, asymptomatic and usually transient serum aminotransferase elevations in approximately 1% of patients, but levels above 3 times the upper limit of normal (ULN) were infrequent and no cases of clinically apparent hepatitis were reported from the preregistration clinical trials. Since marketing of pitavastatin, however, the sponsor has received reports of jaundice, hepatitis and hepatic failure including fatal cases. However, the clinical features and typical course of the liver injury associated with pitavastatin have not been defined in the published literature. On the other hand, the other statins have all been implicated in cases of clinically apparent acute liver injury that typically arise after 1 to 6 months of therapy with either a cholestatic or hepatocellular pattern of serum enzyme elevations. Rash, fever and eosinophilia are uncommon, but some cases have been marked by autoimmune features including autoantibodies, chronic hepatitis on liver biopsy and a clinical response to corticosteroid therapy. This pattern has yet to be shown to apply to pitavastatin.
Adverse effectsThe most commonly reported adverse effects related to pitavastatin use include back pain, constipation, diarrhea, myalgia, and pain in the extremities. Reports exist of rash, pruritus, and urticaria. There are also reports of myopathy and rhabdomyolysis, leading to acute renal failure. Pitavastatin use can also cause lab abnormalities, including elevated creatine phosphokinase, transaminases (aspartate aminotransferase [AST]/serum glutamic-oxaloacetic transaminase, or alanine aminotransferase [ALT]/serum glutamic-pyruvic transaminase), alkaline phosphatase, bilirubin, and glucose. High fasting serum glucose levels and high HgA1c levels have also occurred with pitavastatin use.
Toxicity summaryIDENTIFICATION AND USE: Pitavastatin, a hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitor (i.e., statin), is an antilipemic agent. It is used as an adjunct to lifestyle modifications for the management of dyslipidemias. HUMAN EXPOSURE AND TOXICITY: Pitavastatin is contraindicated for use in pregnant women or patients with active liver disease, including unexplained, persistent elevations in serum aminotransferase concentrations. Cases of myopathy and rhabdomyolysis with acute renal failure secondary to myoglobinuria have been reported with HMG-CoA reductase inhibitors, including pitavastatin. These risks can occur at any dose level, but increase in a dose-dependent manner. Cases of fatal and nonfatal hepatic failure have also been reported rarely in patients receiving pitavastatin. ANIMAL STUDIES: In a 92-week carcinogenicity study in mice given pitavastatin, at the maximum tolerated dose of 75 mg/kg/day there was an absence of drug-related tumors. However, in a 92-week carcinogenicity study in rats given pitavastatin at 1, 5, 25 mg/kg/day by oral gavage, there was a significant increase in the incidence of thyroid follicular cell tumors at 25 mg/kg/day. Embryo-fetal developmental studies were conducted in pregnant rats treated with 3, 10, 30 mg/kg/day pitavastatin by oral gavage during organogenesis. No adverse effects were observed at 3 mg/kg/day. Embryo-fetal developmental studies were conducted in pregnant rabbits treated with 0.1, 0.3, 1 mg/kg/day pitavastatin by oral gavage during the period of fetal organogenesis. Maternal toxicity consisting of reduced body weight and abortion was observed at all doses tested. In perinatal/postnatal studies in pregnant rats given oral gavage doses of pitavastatin at 0.1, 0.3, 1, 3, 10, 30 mg/kg/day from organogenesis through weaning, maternal toxicity consisting of mortality at 0.3 mg/kg/day and impaired lactation at all doses contributed to the decreased survival of neonates in all dose groups. Pitavastatin had no adverse effects on male and female rat fertility at oral doses of 10 and 30 mg/kg/day, respectively. Pitavastatin was not mutagenic in the Ames test with Salmonella typhimurium and Escherichia coli with and without metabolic activation, the micronucleus test following a single administration in mice and multiple administrations in rats, the unscheduled DNA synthesis test in rats, and a Comet assay in mice. In the chromosomal aberration test, clastogenicity was observed at the highest doses tested which also elicited high levels of cytotoxicity.A common side effect of pitavastatin toxicity is myalgia. In the setting of overdose, there is no known treatment. Patients should be provided with supportive measures and should receive treatment for any symptoms. Given the high protein binding ratio of pitavastatin, hemodialysis would not be beneficial.
Human Toxicity Excerpts/SIGNS AND SYMPTOMS/ Cases of myopathy and rhabdomyolysis with acute renal failure secondary to myoglobinuria have been reported with HMG-CoA reductase inhibitors, including Livalo. These risks can occur at any dose level, but increase in a dose-dependent manner./SIGNS AND SYMPTOMS/ Cases of fatal and nonfatal hepatic failure have been reported rarely in patients receiving statins, including pitavastatin, during postmarketing surveillance./EPIDEMIOLOGY STUDIES/ ... We conducted a meta-analysis and employed indirect comparisons to identify differing risk effects across statins. We included any randomized clinical trial (RCT) of atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin and simvastatin used for cardiovascular disease event prevention. The main outcome was adverse events [all-cause mortality, cancers, rhabdomylosis, diabetes, aspartate and alanine aminotransferase (AST/ALT), and creatinine kinase (CK) increases beyond the upper limit of normal]. In order to evaluate the relative effects of each drug on adverse events, we calculated adjusted indirect comparisons of the adverse-event outcomes. Seventy-two trials involving 159,458 patients met our inclusion criteria. Overall, statin treatments significantly increased the rate of diabetes when compared to controls (OR: 1.0995% CI: 1.02-1.16) and elevated AST (OR: 1.3195% CI: 1.04-1.66) and ALT (OR: 1.2895% CI: 1.11-1.48) levels when compared to controls. Using indirect comparisons, we also found that atorvastatin significantly elevated AST levels compared to pravastatin (OR: 2.2195% CI: 1.13-4.29) and simvastatin significantly increased CK levels when compared to rosuvastatin (OR: 4.3995% CI: 1.01-19.07). Higher dose studies had increased risk of AST elevations. Although statins are generally well tolerated, there are risks associated with almost all drugs. With few exceptions, statins appear to exert a similar risk across individual drugs./ALTERNATIVE and IN VITRO TESTS/ /The purpose of this study was/ to determine the effect of different statins on the induction of diabetes mellitus. Four statins (atorvastatin, pravastatin, rosuvastatin, and pitavastatin) were used. Cytotoxicity, insulin secretion, glucose-stimulated insulin secretion, and G0/G1 phase cell cycle arrest were investigated in human pancreas islet beta cells, and glucose uptake and signaling were studied in human skeletal muscle cells (HSkMCs). Human pancreas islet beta cells treated with 100 nM atorvastatin, pravastatin, rosuvastatin, and pitavastatin had reduced cell viability (32.12%, 41.09%, 33.96%, and 29.19%, respectively) compared to controls. Such cytotoxic effect was significantly attenuated by decreasing the dose to 10 and 1 nM, ranged from 1.46% to 17.28%. Cells treated with 100 nM atorvastatin, pravastatin, rosuvastatin, and pitavastatin had a reduction in the rate of insulin secretion rate by 34.07%, 30.06%, 26.78%, and 19.22%, respectively. The inhibitory effect was slightly attenuated by decreasing the dose to 10 and 1 nM, ranging from 10.84% to 29.60%. Insulin secretion stimulated by a high concentration of glucose (28 mmol/L) was significantly higher than a physiologic concentration of glucose (5.6 mmol/L) in all treatment groups. The glucose uptake rates at a concentration of 100 nM were as follows: atorvastatin (58.76%) < pravastatin (60.21%) < rosuvastatin (72.54%) < pitavastatin (89.96%). We also found that atorvastatin and pravastatin decreased glucose transporter (GLUT)-2 expression and induced p-p38 MAPK levels in human pancreas islet beta cells. Atorvastatin, pravastatin, and rosuvastatin inhibited GLUT-4, p-AKT, p-GSK-3beta, and p-p38 MAPK levels in HSkMCs. Statins similar but different degree of effects on pancreas islet beta cells damage and induce insulin resistance in HSkMC.For more Human Toxicity Excerpts (Complete) data for Pitavastatin (9 total), please visit the HSDB record page.
Non-Human Toxicity Excerpts/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ In a 26-week transgenic mouse (Tg rasH2) carcinogenicity study where animals were given pitavastatin at 30, 75, and 150 mg/kg/day by oral gavage, no clinically significant tumors were observed./LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ In a 92-week carcinogenicity study in mice given pitavastatin, at the maximum tolerated dose of 75 mg/kg/day with systemic maximum exposures (AUC) 26 times the clinical maximum exposure at 4 mg/day, there was an absence of drug-related tumors./LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ The effects of (+)-monocalcium bis((3R,5S,6E)-7-(2-cyclopropyl-4-(4-fluorophenyl)-3-quinolyl)-3,5-dihydroxy-6- heptenoate) (NK-104), a novel HMG-CoA reductase inhibitor, on fertility of parent animals and fetal development were studied in Crj:CD(SD) rats. NK-104 was administered orally at daily dose levels of 2, 10 and 30 mg/kg. Males were treated with NK-104 for 70 days prior to mating, during the 3-week mating period and for about 7 days until the day of terminal sacrifice. Initially, 50 mg/kg of NK-104 was given to the highest dose group of males for the first 36 days of premating period. Three rats, however, died during this period. Therefore, thereafter the dose level was lowered from 50 mg/kg to 30 mg/kg in the highest dose group. Females were treated for 14 days prior to mating, during the mating period and through day 7 of gestation. Among the parent animals, reduced body weight gain and decreased food intake were noted in the male maximum dose group during the period given 50 mg/kg, and 3 animals died on days 14, 21 and 23 of premating period. The reduced body weight gain and decrease of food intake were noted to continue after the dose level was reduced to 30 mg/kg. At autopsy, white discoloration and thickening of the forestomach mucosa were observed in this group. No treatment-related effects were observed on general condition, body weight, food intake or gross pathology in the female groups. Examinations on the parent animals revealed no adverse effects of NK-104 on the parameters of reproductive function such as estrous cycle, copulation index, fertility index or number of corpora lutea. No treatment-related effects were observed in any groups on the number of implantations, implantation index, fetal mortality, number of live fetuses, sex ratio, fetal weight, placental appearance, placental weight, properties of amniotic fluid or externals. Based on these results, it is concluded that the non-toxic dose of NK-104 was 10 mg/kg for general toxicity in parent animals and 30 mg/kg for reproductive function of parent animals and for fetuses./LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ In a 92-week carcinogenicity study in rats given pitavastatin at 1, 5, 25 mg/kg/day by oral gavage there was a significant increase in the incidence of thyroid follicular cell tumors at 25 mg/kg/day, which represents 295 times human systemic exposures based on AUC at the 4 mg/day maximum human dose.For more Non-Human Toxicity Excerpts (Complete) data for Pitavastatin (10 total), please visit the HSDB record page.
Populations at Special RiskLivalo is contraindicated in women who are or may become pregnant. Serum cholesterol and triglycerides (TG) increase during normal pregnancy, and cholesterol products are essential for fetal development.Pitavastatin should be used with caution in patients who consume substantial amounts of alcohol. The drug is contraindicated in patients with active liver disease, including unexplained, persistent elevations in serum aminotransferase concentrations.
Antidote and Emergency Treatment/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B//SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B//SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W TKO /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/There is no known specific treatment in the event of overdose of pitavastatin. In the event of overdose, the patient should be treated symptomatically and supportive measures instituted as required. Hemodialysis is unlikely to be of benefit due to high protein binding ratio of pitavastatin.
Effects During Pregnancy and Lactation◉ Summary of Use during Lactation
Signal wordWarning
GHS pictogramGHS07
GHS hazard statementsH302-H315-H319-H335
GHS precautionary statementsP261-P305+P351+P338
Hazardous substances data147511-69-1(Hazardous Substances Data)