体外活性：吉非贝齐对 CYP3A 介导的辛伐他汀羟基酸 (SVA) 氧化具有最小的抑制作用，但在狗和人肝微粒体中抑制 SVA 葡萄糖醛酸化。吉非贝齐显着抑制 M-23 形成，K(i) (IC(50)) 值为 69 (95) mM，而对 M-1 形成的抑制较弱，K(i) (IC(50)) 值人肝微粒体中的浓度为 273 mM。 Gembrozil 强烈且竞争性地抑制 CYP2C9 活性，K(i) (IC(50)) 值为 5.8 (9.6) mM。吉非贝齐对 CYP2C19 和 CYP1A2 活性的抑制作用稍小，K(i) (IC(50)) 值分别为 24 (47) mM 和 82 (136) mM。吉非贝齐是一种降脂药物，可抑制人 U373MG 星形胶质细胞和原代星形胶质细胞中细胞因子诱导的 NO 产生和诱导型一氧化氮合酶 (iNOS) 的表达。吉非贝齐诱导过氧化物酶体增殖物反应元件 (PPRE) 依赖性荧光素酶活性，该活性受到 DeltahPPAR-α（人 PPAR-α 的显性失活突变体）表达的抑制。吉非罗齐强烈抑制 NF-kappaB、AP-1 和 C/EBPbeta 的激活，但不抑制细胞因子刺激的星形胶质细胞中 γ 激活位点 (GAS) 激酶测定：CYP3A4（睾酮 6β-羟基化）和 CYP2C8 的活性（紫杉醇 6α-羟基化）的测定。使用的标记底物浓度（25 μM 睾酮和 1 至 5 μM 紫杉醇）与反应的 Km 值相当或接近。在与人肝微粒体 (0.1 mg/mL) 启动反应之前，将吉非罗齐与标记底物和 NADPH (1 mM) 在 37°C 下共孵育 15 分钟，或者与人肝微粒体和 NADPH 预孵育 15 分钟，然后添加标记基底。细胞测定：简而言之，将400μL培养上清液与200μL Griess试剂反应并在室温下孵育15分钟。测定样品的光密度通过分光光度法在 570 nm 处测量。新鲜培养基作为所有实验中的空白。亚硝酸盐浓度根据测定中 NaNO2 反应得出的标准曲线计算。

吉非罗齐治疗显着降低（2-3倍）SVA的血浆清除率和SVA葡萄糖醛酸苷（连同其环化产物SV）的胆汁排泄，但不降低狗中SVA主要氧化代谢物的排泄。

Absorption, Distribution and Excretion
Gemfibrozil is absorbed from the gastrointestinal tract. In healthy volunteers, a 900mg oral dose of gemfibrozil has a Cmax of 46±16µg/mL with a Tmax of 2.2±1.1h. In patients with chronic renal failure, gemfibrozil has a Cmax of 13.8±11.1µg/mL with a Tmax of 2.3±1.0h. In patients with liver disease, gemfibrozil has a Cmax of 23.0±10.3µg/mL with a Tmax of 2.6±1.7h.
Approximately 70% of a dose of gemfibrozil is eliminated in the urine. The majority of a dose is eliminated as a glucuronide conjugate and <2% is elimiinated as the unmetabolized drug. 6% of a dose is eliminated in the feces. In healthy volunteers, 0.02-0.15% of a dose was detected in the urine as unmetabolized gemfibrozil, with 7-14% detected as conjugated metabolites. In patients with renal failure, trace amounts of unmetabolized gemfibrozil is present in the urine, with 0.5-9.8% detected as conjugated metabolites. In patients with liver disease, 0.1-0.2% of a dose was detected in the urine as unmetabolized gemfibrozil, with 25-50% detected as conjugated metabolites.
The volume of distribution of gemfibrozil is estimated to be 0.8L/kg.
The clearance of gemfibrozil is estimated to be 6.0L/h.
Studies in monkeys indicate that gemfibrozil crosses the placenta.
About 95% of gemfibrozil is protein bound. In vitro at concentrations of 0.1-12 ug/mL, 97% of gemfibrozil is bound to 4% human serum albumin; the major metabolite of gemfibrozil (metabolite III) has no effect on the binding capacity of gemfibrozil.
In animals, maximum tissue concentrations of gemfibrozil were reached 1 hour after administration of a single dose, and highest concentrations occurred in liver and kidneys.
Gemfibrozil is rapidly and completely absorbed from the GI tract. The relative bioavailability of gemfibrozil capsules compared with an oral solution of the drug is 97%. The drug undergoes enterohepatic circulation. Plasma gemfibrozil concentrations show marked interindividual variability but tend to increase proportionally with increasing dose. Plasma concentrations of the drug do not appear to correlate with therapeutic response. Following single or multiple oral doses of gemfibrozil, peak plasma concentrations of the drug occur within 1-2 hours. Following oral administration of a single 800-mg dose in healthy adults in one study, mean peak plasma gemfibrozil concentrations of 33 ug/mL occurred 1-2 hours after ingestion. Following oral administration of multiple doses of the drug (600 mg twice daily) in healthy adults in another study, mean peak plasma concentrations of the drug were 16-23 ug/mL about 1-2 hours after a dose.
For more Absorption, Distribution and Excretion (Complete) data for Gemfibrozil (9 total), please visit the HSDB record page.

---

Metabolism / Metabolites
Gemfibrozil undergoes hydroxylation at the 5'-methyl and 4' positions to form the M1 and M2 metaolites respectively. Gemfibrozil also undergoes O-glucuronidation to form gemfibrozil 1-beta glucuronide, an inhibitor of CYP2C8. This O-glucuronidation is primarily mediated by UGT2B7, but also by UGT1A1, UGT1A3, UGT1A9, UGT2B4, UGT2B17.
Gemfibrozil is biotransformed extensively following oral administration. A major pathway of gemfibrozil metabolism is via glucuronidation. Following a single oral administration of 450 mg (6 mg/kg bw est) gemfibrozil to six male subjects, gemfibrozil glucuronide represented approximately 50% of the total urinary metabolites (32% of the dose) recovered within 24 hr. Very similar results had been obtained in /another/ ... study, in which 31% of the dose was recovered as urinary gemfibrozil glucuronide over 0-48 hr. Among metabolites resulting from phase I biotransformation, 5-(5-carboxy-2-methylphenoxy)-2,2-dimethyl pentanoic acid (M3) was the major metabolite recovered. ... A 24-hr urine collection contained both free and conjugated M3 at approximately 15% and 5% of the total dose, respectively, while, in /another/ study, free and conjugated M3 represented approximately 7% and 5% of the recovered radiactivity, respectively. Other minor metabolites identified were the 5-hydroxymethyl derivative (M2, an intermediate in the pathway to M3), a 4-hydroxy derivative (M1) and a 2- hydroxymethyl derivative (M4). In aggregate, urinary and fecal excretion of radioactivity accounted for 66% and 6%, respectively, of the elimination of orally administered gemfibrozil over five days.
The exact metabolic fate of gemfibrozil has not been fully elucidated, but the drug appears to be metabolized in the liver to 4 major metabolites produced via 3 metabolic pathways. Gemfibrozil undergoes hydroxylation of the m-methyl group to the corresponding benzyl alcohol derivative (metabolite II), which is rapidly oxidized to a benzoic acid metabolite (metabolite III, 3-[(4-carboxy-4-methylpentyl)oxy]-4-methylbenzoic acid), the major metabolite. The drug also undergoes hydroxylation of the aromatic ring to produce a phenol derivative (metabolite I) which is probably further metabolized to a compound that is phenolic but has no intact carboxylic acid function (metabolite IV). Metabolite I is pharmacologically active. The drug and its metabolites also undergo conjugation.
The roles of multidrug resistance-associated protein (Mrp) 2 deficiency and Mrp3 up-regulation were evaluated on the metabolism and disposition of gemfibrozil. Results from in vitro studies in microsomes showed that the hepatic intrinsic clearance (CLint) for the oxidative metabolism of gemfibrozil was slightly higher (1.5-fold) in male TR- rats, which are deficient in Mrp2, than in wild-type Wistar rats, whereas CLint for glucuronidation was similar in both strains. The biliary excretion of intravenously administered [14C]gemfibrozil was significantly impaired in TR-) rats compared with Wistar rats (22 versus 93% of the dose excreted as the acyl glucuronides over 72 h). Additionally, the extent of urinary excretion of radioactivity was much higher in TR- than in Wistar rats (78 versus 2.6% of the dose). There were complex time-dependent changes in the total radioactivity levels and metabolite profiles in plasma, liver and kidney, some of which appeared to be related to the up-regulation of Mrp3. Overall, it was demonstrated that alterations in the expression of the transporters Mrp2 and Mrp3 significantly affected the excretion as well as the secondary metabolism and distribution of (14)Cgemfibrozil.
... (14)C-Gemfibrozil was administered orally to rats at a dose of 2000 mg/kg. At various time points, radioactivity in urine was analyzed by liquid scintillation spectrometry, high-pressure liquid chromatography, liquid chromatography/mass spectrometry, gas chromatography/mass spectroscopy, and nuclear magnetic resonance. Nine metabolites of gemfibrozil were identified, some that have not been reported previously. Although the majority of metabolites were glucuronidated, some nonglucuronidated metabolites were identified in urine, including a diol metabolite (both ring methyls hydroxylated), and the product of its further metabolism, the acid-alcohol derivative (ortho ring methyl hydroxylated, meta ring methyl completely oxidized to the acid). Hydroxylation of the aromatic ring also was a common pathway for gemfibrozil metabolism, leading to the production of two phenolic metabolites, only one of which was detected in the urine in the nonconjugated or free form. Also of interest was the finding that both acyl and ether glucuronides were produced, including both glucuronide forms of the same metabolite (e. g., 1-O-GlcUA, 5'-COOH-gemfibrozil, and 5'-COO-GlcUA-gemfibrozil); the positions and functionality of the glucuronide conjugates were identified using base hydrolysis or glucuronidase treatment, in combination with liquid chromatography/MS and nuclear magnetic resonance.
Gemfibrozil has known human metabolites that include (2S,3S,4S,5R)-6-[5-(2,5-Dimethylphenoxy)-2,2-dimethylpentanoyl]oxy-3,4,5-trihydroxyoxane-2-carboxylic acid.
Hepatic. Gemfibrozil mainly undergoes oxidation of a ring methyl group to successively form a hydroxymethyl and a carboxyl metabolite.
Route of Elimination: Approximately seventy percent of the administered human dose is excreted in the urine, mostly as the glucuronide conjugate, with less than 2% excreted as unchanged gemfibrozil.
Half Life: 1.5 hours

---

Biological Half-Life
Gemfibrozil has a plasma half-life of 1.5 hours. In patients with renal failure the half life is 2.4h and in patients with liver disease the half life is 2.1h.
The elimination half-life of gemfibrozil is about 1.5 hours after a single dose and 1.3-1.5 hours after multiple doses in individuals with normal renal function.
The disposition of the lipid-lowering drug gemfibrozil was studied in patients with either renal (n = 8) or hepatic disease (n = 8) and compared to those of healthy volunteers (n = 6). ... Following oral administration of 900 mg gemfibrozil ... the elimination half-life of the drug was 1.5 hr in controls, 2.4 hr in renal failure, and 2.1 hr in liver disease.

Toxicity Summary
Gemfibrozil increases the activity of extrahepatic lipoprotein lipase (LL), thereby increasing lipoprotein triglyceride lipolysis. It does so by activating Peroxisome proliferator-activated receptor-alpha (PPAR‘±) 'transcription factor ligand', a receptor that is involved in metabolism of carbohydrates and fats, as well as adipose tissue differentiation. This increase in the synthesis of lipoprotein lipase thereby increases the clearance of triglycerides. Chylomicrons are degraded, VLDLs are converted to LDLs, and LDLs are converted to HDL. This is accompanied by a slight increase in secretion of lipids into the bile and ultimately the intestine. Gemfibrozil also inhibits the synthesis and increases the clearance of apolipoprotein B, a carrier molecule for VLDL.

---

Hepatotoxicity
Mild, transient serum aminotransferase elevations develop in approximately 20% of patients receiving gemfibrozil, but values above 3 times normal in 5% or less. These abnormalities are usually asymptomatic and transient, resolving even with continuation. However, there have also been rare reports of clinically apparent liver injury in patients on long term gemfibrozil. The clinical presentation was highly variable. The onset of injury varied from a few weeks to several years after starting the medication and the pattern of serum enzyme elevations ranged from hepatocellular (Case 1) to mixed to cholestatic. Cases have not been associated with signs of immunoallergic (fever, rash, eosinophilia) or autoimmune hepatitis and recovery has been prompt and complete with stopping therapy.
Likelihood score: C (probable rare cause of clinically apparent liver injury).

---

Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
No relevant published information exists on the use of gemfibrozil during breastfeeding. Because of a concern with disruption of infant lipid metabolism, gemfibrozil is best avoided during breastfeeding. An alternate drug is preferred, especially while nursing a newborn or preterm infant.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

---

Protein Binding
Gemfibrozil is 99% protein bound. It is 98.6% bound to serum albumin, 0.8% bound to erythrocytes, and 0.8% unbound. There is negligible binding to alpha-1-acid glycoprotein.

---

Toxicity Data
Oral, mouse: LD₅₀ = 3162 mg/kg.

---

Interactions
In a randomized crossover study, 24 SLCO181-genotyped healthy volunteers were given daily doses of 1,200 mg gemfibrozil, 40 mg atorvastatin, or placebo, followed by 0.25 mg of repaglinide on day 3. The mean increase in the repaglinide area under the plasma concentration-time curve from 0 hr to infinity (AUC(0-infinity)) produced by gemfibrozil was larger in individuals with the SLCO1B1 c.521CC genotype (n = 6) than in those with the c.521TC (n = 6) and c.521TT (n = 12) genotypes, by factors of 1.56 (P = 0.004) and 1.54 (P = 0.002), respectively. Gemfibrozil prolonged the repaglinide elimination half-life 1.43 times more in the c.521 CC group than in the c.521TT group (P = 0.047), but no differences were seen in the effects on peak plasma concentration (C(max)). While on gemfibrozil, the minimum blood glucose concentration after repaglinide intake was 19% lower in the c.521CC participants than in the c.521TT participants (P = 0.009). In the c.521TT group, atorvastatin intake had the effect of increasing repaglinide Cmax and AUC(0-infinity) by 41% (P = 0.001) and 18% (P = 0.033), respectively. In conclusion, the extent of gemfibrozil-repaglinide interaction depends on SLCO1B1 genotype. Atorvastatin raises plasma repaglinide concentrations, probably by inhibiting organic anion transporting polypeptide 1B1 (OATP1B1).
... In a randomized crossover study, 12 healthy volunteers received twice daily for 3 days either 600 mg gemfibrozil, 100 mg itraconazole (first dose 200 mg), both gemfibrozil and itraconazole, or placebo. On day 3 they ingested a 0.25 mg dose of repaglinide. Plasma drug and blood glucose concentrations were followed for 7 hr and serum insulin and C-peptide concentrations for 3 hr postdose. Gemfibrozil raised the area under the plasma concentration-time curve (AUC) of repaglinide 8.1-fold (range 5.5- to 15.0-fold; p<0.001) and prolonged its half-life (t(1/2)) from 1.3 to 3.7 hr (p<0.001). Although itraconazole alone raised repaglinide AUC only 1.4-fold (1.1- to 1.9-fold; p<0.001), the gemfibrozil-itraconazole combination raised it 19.4-fold (12.9- to 24.7-fold) and prolonged the t(1/2) of repaglinide to 6.1 hr (p<0.001). Plasma repaglinide concentration at 7 hr was increased 28.6-fold by gemfibrozil and 70.4-fold by the gemfibrozil-itraconazole combination (p<0.001). Gemfibrozil alone and in combination with itraconazole considerably enhanced and prolonged the blood glucose-lowering effect of repaglinide; i.e., repaglinide became a long-acting and stronger antidiabetic. Clinicians should be aware of this previously unrecognised and potentially hazardous interaction between gemfibrozil and repaglinide. Concomitant use of gemfibrozil and repaglinide is best avoided. If the combination is considered necessary, repaglinide dosage should be greatly reduced and blood glucose concentrations carefully monitored.
Concomitant administration of gemfibrozil 600 mg and a single 0.25-mg dose of repaglinide (dosage strength not commercially available in the US) in healthy individuals receiving gemfibrozil 600 mg twice daily for 3 days increased repaglinide AUC by 8.1-fold and prolonged the half-life of repaglinide from 1.3 to 3.7 hours. When both gemfibrozil and itraconazole were co-administered with repaglinide, the AUC of repaglinide was increased 19-fold and repaglinide half-life was prolonged to 6.1 hours. Plasma repaglinide concentration at 7 hours increased 28.6-fold with concomitant gemfibrozil administration and 70.4-fold with concomitant gemfibrozil-itraconazole therapy. Gemfibrozil therapy should not be initiated in patients taking repaglinide, and those taking gemfibrozil should not begin therapy with repaglinide, since such concomitant use may enhance and prolong the hypoglycemic effects of repaglinide. In addition, because of the apparent synergistic inhibitory effect of gemfibrozil and itraconazole on repaglinide metabolism, patients already receiving concomitant therapy with repaglinide and gemfibrozil should not receive itraconazole.
Myopathy and/or fatal or nonfatal rhabdomyolysis has occurred with combined gemfibrozil and statin (e.g., cerivastatin [no longer commercially available], lovastatin) therapy.
For more Interactions (Complete) data for Gemfibrozil (15 total), please visit the HSDB record page.

---

Non-Human Toxicity Values
LD50 Rat oral 479 mg/kg
LD50 Mouse oral 316 mg/kg

J Pharmacol Exp Ther.2002 Jun;301(3):1042-51;Drug Metab Dispos.2001 Nov;29(11):1359-61.

Therapeutic Uses
Gemfibrozil is used to reduce the risk of developing coronary heart disease in patients with type IIb hyperlipoproteinemia without clinical evidence of coronary heart disease (primary prevention) who have an inadequate response to dietary management, weight loss, exercise, and drugs known to reduce LDL-cholesterol and increase HDL-cholesterol (e.g., bile acid sequestrants) and who have low HDL-cholesterol concentrations in addition to elevated LDL-cholesterol and triglycerides. /Included in US product label/
In a randomized, double-blind five-year trial, ... the efficacy of simultaneously elevating serum levels of high-density lipoprotein (HDL) cholesterol and lowering levels of non-HDL cholesterol with gemfibrozil in reducing the risk of coronary heart disease /was examined/ in 4081 asymptomatic middle-aged men (40 to 55 years of age) with primary dyslipidemia (non-HDL cholesterol greater than or equal to 200 mg per deciliter [5.2 mmol per liter] in two consecutive pretreatment measurements). One group (2051 men) received 600 mg of gemfibrozil twice daily, and the other (2030 men) received placebo. Gemfibrozil caused a marked increase in HDL cholesterol and persistent reductions in serum levels of total, low-density lipoprotein (LDL), and non-HDL cholesterol and triglycerides. There were minimal changes in serum lipid levels in the placebo group. The cumulative rate of cardiac end points at five years was 27.3 per 1,000 in the gemfibrozil group and 41.4 per 1,000 in the placebo group--a reduction of 34.0 percent in the incidence of coronary heart disease (95 percent confidence interval, 8.2 to 52.6; P less than 0.02; two-tailed test). The decline in incidence in the gemfibrozil group became evident in the second year and continued throughout the study. There was no difference between the groups in the total death rate, nor did the treatment influence the cancer rates. ...
... To compare the effectiveness and safety of lipid-lowering therapy in patients with and without HIV infection /a/ retrospective cohort study /was conducted in/ 829 patients with HIV infection and 6941 patients without HIV infection beginning lipid-lowering therapy for elevated low-density lipoprotein cholesterol or triglyceride levels. Compared with patients without HIV infection, patients with HIV infection beginning statin therapy had smaller reductions in low-density lipoprotein cholesterol levels (25.6% vs. 28.3%; P = 0.001), which did not vary by antiretroviral therapy class. Patients with HIV infection beginning gemfibrozil therapy had substantially smaller reductions in triglyceride levels than patients without HIV infection (44.2% vs. 59.3%; P < 0.001), and reductions with gemfibrozil varied by antiretroviral therapy class (44.0% [P = 0.001] in patients receiving protease inhibitors only, 26.4% [P < 0.001] in patients receiving protease inhibitors and nonnucleoside reverse transcriptase inhibitors [NNRTIs], and 60.3% [P = 0.94] in patients receiving NNRTIs only). Rhabdomyolysis was diagnosed in 3 patients with HIV infection and 1 patient without HIV infection. No clinically recognized cases of myositis or myopathy were observed. The risk for laboratory adverse events was low (<5%), although it was increased in patients with HIV infection. Limitations: Laboratory measurements were not uniformly performed according to HIV status, and adequate fasting before lipoprotein testing could not be verified. Results may not be completely generalizable to uninsured persons, women, or certain racial or ethnic minorities. Dyslipidemia, particularly hypertriglyceridemia, is more difficult to treat in patients with HIV infection than in the general population. However, patients with HIV infection receiving NNRTI-based antiretroviral therapy and gemfibrozil had triglyceride responses similar to those in patients without HIV infection.
Gemfibrozil is used as an adjunct to dietary therapy for the management of severe hypertriglyceridemia in patients at risk of developing pancreatitis (typically those with serum triglyceride concentrations exceeding 2000 mg/dL and elevated concentrations of VLDL and fasting chylomicrons) who do not respond adequately to dietary management. Gemfibrozil also may be used in patients with triglyceride concentrations of 1000-2000 mg/dL who have a history of pancreatitis or of recurrent abdominal pain typical of pancreatitis; however, efficacy of the drug in patients with type IV hyperlipoproteinemia and triglyceride concentrations less than 1000 mg/dL who exhibit type V patterns subsequent to dietary or alcoholic indiscretion has not been adequately studied. The manufacturer states that gemfibrozil is not indicated for use in patients with type I hyperlipoproteinemia who have elevated triglyceride and chylomicron concentrations but normal VLDL-cholesterol concentrations. /Included in US product label/
For more Therapeutic Uses (Complete) data for Gemfibrozil (6 total), please visit the HSDB record page.

---

Drug Warnings
Adverse effects of gemfibrozil are infrequent and generally mild; however, because of the chemical, pharmacologic, and clinical similarities between clofibrate (no longer commercially available in the US) and gemfibrozil, the possibility that gemfibrozil may share the toxic potentials of clofibrate should be considered.
The most frequent adverse effects of gemfibrozil involve the GI tract and occasionally may be severe enough to require discontinuance of the drug. Abdominal pain (and, in some instances, acute appendicitis), and epigastric pain or dyspepsia are common adverse GI effects reported with gemfibrozil. Nausea, vomiting, diarrhea, constipation, and flatulence occur less frequently; cholestatic jaundice also has been reported. Dry mouth, anorexia and/or weight loss, gas pain, pancreatitis, colitis, and heartburn have also been reported in patients receiving gemfibrozil but have not been directly attributed to the drug.
Headache, dizziness, drowsiness or somnolence, blurred vision, paresthesia, hypesthesia, taste perversion, peripheral neuritis, mental depression, and impotence and decreased libido have been reported in patients receiving gemfibrozil. Although a causal relationship has not been established, vertigo, syncope, insomnia, asthenia, chills, psychic problems, fatigue, confusion, and seizures have also occurred in patients receiving the drug.
Slight decreases in hemoglobin and hematocrit and in leukocyte count have occurred in a few patients receiving gemfibrozil; these levels stabilize during long-term administration. Eosinophilia has also been reported. The drug may also affect blood coagulation. Severe anemia, leukopenia, thrombocytopenia, and bone marrow hypoplasia reportedly have occurred rarely in patients receiving gemfibrozil. Therefore, the manufacturer recommends that blood cell counts be monitored periodically during the first 12 months of therapy.
For more Drug Warnings (Complete) data for Gemfibrozil (19 total), please visit the HSDB record page.

---

Pharmacodynamics
Gemfibrozil alters lipid metabolism to treat patients with hyperlipidemia. The duration of action requires twice daily dosing as the mean residence time of gemfibrozil is up to 9.6h in patients with chronic renal failure. Gemfibrozil has a wide therapeutic index as trials with twice the standard dose were not associated with severe side effects. Patients taking gemfibrozil may be at an increased risk of developing cholelithiasis and cholecystitis, as seen in patients taking [clofibrate].

C15H22O3

250.33

250.156

25812-30-0

Gemfibrozil;25812-30-0

3463

White to off-white solid powder

1.0±0.1 g/cm3

394.7±30.0 °C at 760 mmHg

61-63°C

141.6±18.1 °C

0.0±1.0 mmHg at 25°C

1.512

4.39

46.53

1

3

6

18

273

0

HEMJJKBWTPKOJG-UHFFFAOYSA-N

InChI=1S/C15H22O3/c1-11-6-7-12(2)13(10-11)18-9-5-8-15(3,4)14(16)17/h6-7,10H,5,8-9H2,1-4H3,(H,16,17)

5-(2,5-dimethylphenoxy)-2,2-dimethylpentanoic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)