25812-30-0 Usage
Uses
Used in Pharmaceutical Industry:
Gemfibrozil is used as a lipid-regulating agent for the treatment of hyperlipidemia. It is particularly suitable for patients with severe type IV or type V hyperlipoproteinemia and high-risk coronary heart disease who have not responded to treatments such as dietary control or weight loss. It is also applicable to type II-b hyperlipoproteinemia patients with high-risk coronary heart disease who have failed to respond to treatments like dietary control, weight loss, or other lipid-regulating medications.
Used in Cardiovascular Health:
Gemfibrozil is used as an antihyperlipoproteinemic agent to reduce cholesterol and triglyceride levels in the blood. It significantly lowers very low-density lipoprotein (VLDL) levels and increases high-density lipoprotein (HDL) levels, with little effect on low-density lipoprotein (LDL) levels. It can be used clinically in patients with various lipid metabolism disorders, such as primary and secondary hyperlipoproteinemias, hypercholesterolemias, hypertriglyceridemias, mixed hyperlipidemias, and lipid metabolism disorders caused by diabetes. It is also used to prevent the occurrence of myocardial infarction.
Used in Research:
Gemfibrozil has been used in research to study its effects on cell cycle progression in yeast and to investigate the effects of fibrates on cell proliferation and gene expression in human cell lines.
Brand Names:
Lopid (Pfizer), Gevilon, Hipolixan, Ipolipid, Lipur, Tenorac.
A lipid-regulating agent
Gemfibrozil, with the chemical name known as 2, 2-dimethyl-5-(2, 5-dimethylphenoxy) pentanoic acid, is a lipid-regulating agent belonging to clofibric acid derivatives. Appearing on the American market in 1982, it overcomes the serious side effects that the former hypolipidemic agent clofibrate has had on the liver and retains its effective role. Gemfibrozil can promote peripheral lipolysis, reduce triglyceride formation in the liver by reducing liver uptake of free fatty acids, and reduce very-low-density lipoprotein production by inhibiting the synthesis of very-low-density lipoprotein apolipoprotein. It can lower blood triglycerides and thus increases the level of blood high-density lipoprotein. It can mildly reduce the level of low-density lipoprotein cholesterol in blood. However, it may increase the level of low-density lipoprotein in type IV hyperlipoproteinemia. Controlled studies have shown that gemfibrozil can reduce the occurrences of myocardial infarction and sudden death caused by severe coronary artery disease. The agent is suitable for treatment of severe type IV or type V hyperlipoproteinemia patients with high-risk coronary heart disease who had no response to treatments such as dietary control or weight loss. It is also applicable to type II-b hyperlipoproteinemia patients with high-risk coronary heart disease who had failed to respond to treatments such as dietary control, weight loss, or other lipid-regulating medications.
Synthetic route
Figure 1 is a synthetic route for preparing gemfibrozil
Production method
(1) 1. 1-(2,5-dimethylphenoxy)-3-chloro-propane was obtained by the reaction of 2, 5-dimethylphenol with bromochloropropane. The reaction is carried out in toluene mixed with bromo-geramine in a reflux system for five hours.
2. Lithium isobutyrate was obtained by the reaction of sodium isobutyrate with lithium diisopropyl amine
3. Phenoxy acid was synthesized from 1-(2, 5-dimethylphenoxy)-3-chloro-propane and lithium isobutyrate by mixing the two intermediates slowly at 10-15℃, stirring the mixture for 15 minutes and then warming it till the temperature reaches 30℃ and keeping the reaction for five hours.
(2) Method 1: the reaction of 2, 5-dimethylphenol with 1, 3-dibromopropan was used first to obtain an intermediate 3-(2, 5-dimethylphenoxy) propyl bromide. Then 26.4 g isobutyric acid, 6.0 g magnesium oxide and 250 ml toluene were stirred into a mixture and heated under reflux, and the water formed during the heating process was continuously removed. When there was no more water forming, the solution that contains magnesium isobutyrate was concentrated to half of its original volume, and was then cooled down with an ice bath. To this solution, 31.0 g diisopropyl amine dissolved with 200 ml dry tetrahydrofuran was added first, followed by 179 ml of 1.68 mol/l n-butyllithium in pentane being added. During this period, the reaction solution was maintained at a temperature below 10℃. After 15 minutes, the solution was heated at 30℃ for 0.5 hour, then was cooled down to 0-10℃, and 75.0 g of 3-(2, 5-dimethylphenoxy) propyl bromide was added. After being stirred at room temperature for 18 hours, the solution was diluted with 125 ml of 6 mol/l hydrochloric acid and 250 ml water. Finally, the organic layer was removed and the remaining solution was concentrated and underwent vacuum distillation to give gemfibrozil with a boiling point of 158-159℃ under a vacuum of 2.67 Pa.
The product can also be obtained by the following steps: 51.0 g diisopropyl amine, 23.2 g of 57% sodium hydride in mineral oil suspension and 350 ml tetrahydrofuran were mixed and 44.1 g isobutyric acid was added into the mixture with stirring. When there was no more gas producing, the solution was heated under reflux for 15 min. Then the solution was cooled down to 0℃ and 345 ml of 1.45 mol/l n-butyllithium in pentane was added. After reacting for five hours, the solution was incubated at 30℃ for 0.5 hours, and was cooled down to 0℃ and 122.0 g 3-(2, 5-dimethylphenoxy) propyl bromide was added. After reacting for 1 hour, 500 ml water was added to the solution with stirring. Then the solution was allowed to stand to remove the aqueous layer. The remaining solution was acidified with 6mol/l hydrochloric acid and the acidic solution was extracted with ether. The extract was washed with saturated salt water, dried with anhydrous magnesium sulfate, and concentrated almost to dryness and then undergo vacuum distillation. The fraction was collect at 158-159℃ under a vacuum of 2.67 Pa, and was crystallized from hexane to give gemfibrozil of melting point 61-63℃. In the above-described method 4.4 g lithium hydride can be used to replace the sodium hydride.
Method 2: isobutyl isobutyrate was used to react with 1-chloro-3-bromopropane in the presence of lithium diisopropyl amide to produce an intermediate 5-chloro-2, 2-dimethyl-pentanoic acid isobutyl ester. The intermediate was then used to reacts with 2, 5-dimethyl phenol and in the meanwhile generated gemfibrozil by hydrolysis reaction.
Side effects
1. The most common adverse reactions were gastrointestinal discomfort, such as indigestion, anorexia, nausea, vomiting, a sense of fullness, and stomach discomfort; other less common adverse reactions were headache, dizziness, fatigue, skin rashes, itching, impotence, etc.
2. Occasional adverse reactions include cholelithiasis and myositis (muscle pain, or fatigue). This product belongs to clofibric acid derivatives which may cause myositis, myopathy and rhabdomyolysis, leading to elevated blood creatine-phosphokinase. The syndrome of rhabdomyolysis caused mainly showed myalgia accompanied with elevated blood creatine-phosphokinase and myoglobinuria, and in rare cases, can lead to renal failure. It may increase the risk of myopathy in patients with nephrotic syndrome or with other kidney damage that causes hypoalbuminemia, or in patients with hyperthyroidism.
3. Abnormalities in liver function tests (blood aminotransferase, lactate dehydrogenase, bilirubin, increased alkaline phosphatase) were found occasionally, which should return to normal after treatment.
4. Mild anemia and decreased white blood cell count were found occasionally, which should be stable after long term of use; occasions of severe anemia, leukopenia, thrombocytopenia, or bone marrow suppression was found quite rare.
Contraindications
1. Patients who are allergic to the product are contraindicated.
2. Patients with gallbladder disease or cholelithiasis are contraindicated. The agent may exacerbate the symptoms of gallbladder disease.
3. Patients with liver dysfunction or with primary biliary cirrhosis of the liver are contraindicated. The agent may promote the excretion of cholesterol and raise the level of cholesterol from high to higher.
4. Patients with severe renal insufficiency are contraindicated to use the agent as it may cause rhabdomyolysis and severe hyperkalemia.
5. Patients with decreased serum protein caused by nephrotic syndrome are contraindicated to use the agent as it may increase the risk of myopathy.
Precautions
1. This product may interfere with the diagnosis and cause: ① decreases in hemoglobin levels, hematocrit values and white blood cell counts, and ② increases in blood creatine-kinase, alkaline phosphatase, aminotransferase and lactate dehydrogenase.
2. During the medication the following should be checked regularly: ① blood and platelet counts, ② liver function tests, ③ lipids, and ④ blood creatine-phosphokinase.
3. Stop using the agent if the treatment is invalid after three months of therapy, or if there is any other syndrome such as cholelithiasis, significant abnormality in liver function, suspected myopathy symptoms (e.g. muscle pain, tenderness, fatigue, etc.), or significant elevated levels of blood creatine-phosphokinase being found clinically after treatment.
4. Levels of blood cholesterol and triglycerides may rebound above the original level after withdrawal of medication, and thus patients should take low-fat diet and keep monitoring the blood lipid till it returns to normal levels.
5. A variety of primary diseases that cause high blood lipid levels such as hypothyroidism and diabetes need attention and treatment during the treatment of high blood cholesterol. However, for certain medications such as estrogens, thiazide diuretics, and β-blockers which may also cause high blood lipid levels, patients do not need corresponding anti-hyperlipidemic therapy after withdrawal.
6. The agent has been classified as a level-C drug by the U.S. FDA's classifications of medications in pregnancy
7. In view of its potential carcinogenic risks, the agent should be used strictly within the specified range of indications, and should be promptly discontinued when the treatment effect is not obvious.
Drug Interactions
1. The product can obviously enhance the effect of oral anticoagulant drugs. When an oral anticoagulant is given in conjunction with gemfibrozil, the dosage of the oral anticoagulant should be reduced and the prothrombin time should be monitored frequently in order to adjust the dose of the anticoagulant. Its mechanism of action is unclear, which might be related to the product’s ability to replace warfarin from its binding site on the protein and enhances the role correspondingly.
2. The product, when used concomitantly with other protein-bound drugs such as furosemide, phenytoin, tolbutamide, and other sulfonylurea drugs, can also replace those drugs from the protein binding sites and thus enhance their roles. Doses of the above-mentioned drugs should be adjusted when they are taken during the lipid-lowering therapy.
3. Clofibric acid derivatives when used in combination with HMG-CoA reductase inhibitors such as lovastatin for the treatment of hyperlipidemia may increase the risks of severe muscle toxicity by both drugs, causing myopathy syndromes such as myalgia, rhabdomyolysis, and elevated blood creatine-phosphokinase, and thus should be avoided in combination.
4. Gemfibrozil, when used in combination with a bile acid-binding resin such as colestipol, should be taken at least two hours before, or after, taking the bile acid-binding resin, as the bile acid-binding resin can combine with other drugs if they are taken simultaneously and thereby affecting the absorption.
5. This product is mainly excreted by the kidneys. When it is used in combination with immunosuppressive agents such as cyclosporine, it can increase the plasma concentration of the latter as well as renal toxicity, leading to the risk of deterioration of renal function. Therefore, the immunosuppressive agent should be reduced in dose or discontinued during the therapy. Cautions should also be taken when using gemfibrozil concomitantly with other nephrotoxic drugs.
Originator
Lopid,Warner Lambert,US,1982
Manufacturing Process
With stirring, 44.1 g of isobutyric acid is added to a mixture of 51.0 g of
diisopropylamine, 23.2 g of a 57% sodium hydride dispersion in mineral oil,
and 350 ml of tetrahydrofuran. When gas evolution subsides, the mixture is
heated at reflux for 15 minutes, cooled to 0°C, and treated with 345 ml of a
1.45M solution of n-butyl lithium in heptane. After 5 hr, the mixture is
warmed one-half hour at 30°C, cooled to 0°C, and treated with 122.0 g of 3-
(2,5-xylyloxy)propyl bromide. After one more hour, it is stirred with 500 ml of
water and the aqueous phase is separated and acidified with 150 ml of 6N hydrochloric acid. The acidic mixture is extracted with ether and the ether
extract is washed with saturated sodium chloride solution, dried over
magnesium sulfate, concentrated almost to dryness, and distilled in vacuo. A
distillate of 2,2-dimethyl-5-(2,5-xylyloxy)valeric acid is collected at boiling
point 158°C to 159°C at 0.02 mm of Hg; melting point 61°C to 63°C following
crystallization from hexane.
The same product is obtained by substituting 4.4 g of lithium hydride for the
sodium hydride in the above procedure.
The same product is also obtained in the following manner. A mixture of 26.4
g of isobutyric acid, 6.0 g of magnesium oxide powder, and 250 ml of toluene
is stirred and heated at reflux with continuous removal of the water formed in
the reaction. When water formation ceases, the resulting mixture containing
magnesium isobutyrate is concentrated to one-half its original volume, cooled
in an ice bath, and treated with 31.0 g of diisopropylamine in 200 mi of dry
tetrahydrofuran and then with 179 ml of 1.68M n-butyl lithium in heptane
while the temperature is maintained below 10°C. After 15 more minutes, the
mixture is warmed at 30°C for one-half hour, cooled to 0°C to 10°C, and
treated with 75.0 g of 3-(2,5-xylyloxy)propyl bromide. The mixture is then
stirred for 18 hr at room temperature and diluted with 125 ml of 6N
hydrochloric acid and 250 ml of water. The organic phase is separated,
concentrated, and the residue distilled in vacuo to give 2,2-dimethyl-5-(2,5-
xylyloxy)valeric acid.
Therapeutic Function
Antihyperlipidemic
World Health Organization (WHO)
Gemfibrozil, an antihyperlipidaemic derivative of clofibrate, was
introduced in the early 1980's. It is registered in several countries for the treatment
of hyperlipidaemia unresponsive to dietary measures. (See also the WHO comment
for clofibrate).
Biochem/physiol Actions
Gemfibrozil selectively increases Apolipoprotein A-I levels. In yeast cells, application of gemfibrozil delays the start of DNA replication. It is used as a therapeutic agent for dyslipidemia.
Mechanism of action
From the chemical point of view, gemfibrozil is somewhat related to clofibrate and has
analogous pharmacological use. The primary action of gemibrozil as well as clofibrate
consists of a significant reduction in the level of very low-density proteins in the plasma
and an increase in high-density protein formation.
Clinical Use
Hyperlipidaemias of types IIa, IIb, III, IV and V
Synthesis
Gemfibrozil, 2,2-dimethyl-5-(2,5-dimethylphenoxy)valeric acid (20.2.4), is
synthesized either by hydrolysis of ethyl ester of 2,2-dimethyl-5-(2,5-dimethylphenoxy)
valeric acid (20.2.3), which is synthesized by alkylation 2,2-dimethylvaleric acid ethyl ester with 3-(2,5-dimethylphenoxy)propylbromide-1 in the presence of lithium diisopropylamide,
or by oxidation of the corresponding aldehyde (20.2.4).
Veterinary Drugs and Treatments
Gemfibrozil may be useful to reduce serum triglycerides in those
dogs or cats with hypertriglyceridemia and when diet modifications
alone have been unsuccessful. One reference (Elliott 2005)
suggests not adding drug therapy to treat hypertriglyceridemia unless
the serum triglyceride concentration exceeds 500 mg/dL with
associated clinical signs.
Drug interactions
Potentially hazardous interactions with other drugs
Antibacterials: increased risk of myopathy with
daptomycin - try to avoid concomitant use.
Anticoagulants: enhances effect of coumarins and
phenindione; dose of anticoagulant should be reduced
by up to 50% and adjusted by monitoring INR.
Antidiabetics: may improve glucose tolerance and
have an additive effect with insulin or sulphonylureas;
possibly enhanced effect with nateglinide; increased
risk of severe hypoglycaemia with repaglinide - avoid.
Antivirals concentration of paritaprevir increased -
avoid.
Ciclosporin: Parke-Davis have one report on file
of an interaction with ciclosporin where serum
ciclosporin levels were decreased. No effects on
muscle were noted.
Colchicine: possible increased risk of myopathy.
Cytotoxics: bexarotene concentration increased
- avoid; concentration of enzalutamide increased -
avoid or halve enzalutamide dose.
Lipid-regulating drugs: increased risk of myopathy
in combination with statins and ezetimibe - avoid
(maximum 20 mg of rosuvastatin).
Metabolism
Gemfibrozil undergoes oxidation of a ring methyl group
to form successively a hydroxymethyl and a carboxyl
metabolite (the main metabolite). This metabolite
has a low activity compared to the mother compound
gemfibrozil and an elimination half-life of approximately
20 hours.
Gemfibrozil is eliminated mainly by metabolism.
Approximately 70% of the administered human dose is
excreted in the urine, mainly as conjugates of gemfibrozil
and its metabolites. Less than 6% of the dose is excreted
unchanged in the urine; 6% of the dose is found in faeces.
Check Digit Verification of cas no
The CAS Registry Mumber 25812-30-0 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 2,5,8,1 and 2 respectively; the second part has 2 digits, 3 and 0 respectively.
Calculate Digit Verification of CAS Registry Number 25812-30:
(7*2)+(6*5)+(5*8)+(4*1)+(3*2)+(2*3)+(1*0)=100
100 % 10 = 0
So 25812-30-0 is a valid CAS Registry Number.
InChI:InChI=1/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)
25812-30-0Relevant articles and documents
Aryloxycyclohexyl amide AMPK agonist as well as preparation method and medical application thereof
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, (2022/04/06)
The invention discloses an aryloxy cyclohexyl amide AMPK agonist as well as a preparation method and medical application thereof. The AMPK agonist is specifically an aryloxy cyclohexyl amide compound as shown in a formula (I) or pharmaceutically acceptable salt or ester or solvate of the aryloxy cyclohexyl amide compound. The aryloxy cyclohexyl amide compound with the AMPK agonistic activity has remarkable agonistic activity on AMPK at the cellular level, and can effectively activate an AMPK signal channel in vivo, so that the aryloxy cyclohexyl amide compound can be used for preparing medicines for preventing or treating various AMPK-mediated diseases.
Synthesis method for SIPI7623 metabolite of FXR antagonist
-
, (2020/07/15)
The invention provides a synthesis method for an SIPI7623 metabolite, belonging to the field of drug synthesis. The synthesis method has the advantages of reasonable process design, simple operation method and high purity of a prepared target product. The synthesis method comprises the following steps: taking 2,5-dimethylphenol as an initial raw material, then carrying out a nucleophilic substitution reaction, a hydrolysis reaction, an amide condensation reaction and glycosyl modification, and carrying out a hydrolysis reaction so as to obtain a target molecule. The synthesis method provided by the invention is reasonable in route design; and a target product prepared by using the synthesis method provided by the invention provides a test sample for research of the metabolic mechanism of SIPI7623 and has an important value in clinical pharmacokinetic research.
Gemfibrozil hapten, artificial antigen and antibody and preparation method thereof and purpose thereof
-
Paragraph 0024-0029, (2019/02/04)
The invention provides a gemfibrozil hapten and an artificial antigen. Molecular structural formulas of the gemfibrozil hapten and the artificial antigen are correspondingly as shown in the description. The invention further discloses preparation methods for the gemfibrozil hapten, the artificial antigen and an antibody prepared from the gemfibrozil hapten and the artificial antigen and purposes of the gemfibrozil hapten and the antibody. The antibody which is finally prepared by the preparation method provided by the invention has the advantages of high detection sensitivity and high specificity.
Organocatalyzed Aerobic Oxidation of Aldehydes to Acids
Dai, Peng-Fei,Qu, Jian-Ping,Kang, Yan-Biao
supporting information, p. 1393 - 1396 (2019/02/26)
The first example organocatalyzed aerobic oxidation of aldehydes to carboxylic acids in both organic solvent and water under mild conditions is developed. As low as 5 mol % N-hydroxyphthalimide was used as the organocatalyst, and molecular O2 was used as the sole oxidant. No transition metals or hazardous oxidants or cocatalysts were involved. A wide range of carboxylic acids bearing diverse functional groups were obtained from aldehydes, even from alcohols, in high yields.
Synthesis, characterization and evaluation of gemfibrozil-stilbene hybrid as antioxidant agent
Amoroso, Rosa,Leporini, Lidia,Cacciatore, Ivana,Marinelli, Lisa,Ammazzalorso, Alessandra,Bruno, Isabella,De Filippis, Barbara,Fantacuzzi, Marialuigia,Maccallini, Cristina,Menghini, Luigi,Di Stefano, Antonio,Giampietro, Letizia
, p. 1230 - 1238 (2018/11/01)
Background: Oxidative stress and inflammation are important processes involved in cardiovascular disease. Antioxidant agents, like drugs or natural products from plants or plant-based food, represent a promising approach to treat these pathologies. Methods: In light of this, a gemfibrozil-stilbene hybrid (GEM-STIL) was synthesized as a strategy to combine the well-known antioxidant activity of stilbenes with the reported antioxidant and anti-inflammatory actions of fibrates such as gemfibrozil. The physicochemical properties, including aqueous solubility, partition coefficient, chemical stability and enzymatic hydrolysis of GEM-STIL have been studied and indicated that it is stable and has a good lipophilicity. The biological activity was also evaluated for its effect on C2C12 cell line viability and antioxidant activities. Results: The results indicated that GEM-STIL was well tolerated and induced a reduction of cell viability only at higher concentration (100 μg/ml). On the other hand, also at lower nontoxic concentrations (5, 25 and 50 μg/ml) exhibited a significant reduction of ROS production as well as a protective effect against the induced oxidative stimulus. Conclusion: These findings suggest that GEM-STIL is a potential new antioxidant agent useful in oxidative stress-related pathologies.
An improved new path to synthesize gemfibrozil
Nunna, Rambabu,Jayanna,Ramachandran
, p. 925 - 928 (2015/02/05)
A new route has been developed for synthesis of gemfibrozil in good yield with high purity. The obtained gemfibrozil was characterized by using IR, 1H NMR, 13C NMR and mass spectral studies. According to Biopharmaceutical Classification System, gemfibrozil is classified under class-II drugs (low solubility-high permeability) and an antihyperlipidimic. So it's admirable to synthesize the intention molecule in easy and economical way.
Improved process for preparation of gemfibrozil, an antihypolipidemic
Madasu, Suri Babu,Vekariya,Velladurai, Hero,Islam, Aminul,Sanasi, Paul Douglas,Korupolu, Raghu Babu
, p. 963 - 966 (2013/08/23)
An improved process for the preparation of gemfibrozil, an antihypolipodimic drug substance, with an overall yield of 80% and ～99.9% purity (including three chemical reactions) is reported. Formation and control of possible impurities are also described.
Synthesis, characterization and in vitro hydrolysis of a gemfibrozil-nicotinic acid codrug for improvement of lipid profile
Qandil, Amjad M.,Rezigue, Meriem M.,Tashtoush, Bassam M.
experimental part, p. 99 - 108 (2012/03/11)
Combination therapy of fibrates and nicotinic acid has been reported to be synergistic. Herein, we describe a covalent codrug of gemfibrozil (GEM) and nicotinic acid (NA) that was synthesized and characterized by 1H NMR, 13C NMR, FT-IR, MS analysis and elemental analysis. A validated HPLC method was developed that allows for the accurate quantitative determination of the codrug and its hydrolytic products that are formed during the in vitro chemical and enzymatic hydrolysis. The physico-chemical properties of codrug were improved compared to its parent drugs in term of water solubility and partition coefficient. The kinetics of hydrolysis of the codrug was studied using accelerated hydrolysis experiments at high temperatures in aqueous phosphate buffer solution in pH 1.2, 6.8 and 7.4. Using the Arrhenius equation, the extrapolated half-life at 37°C were 289 days at pH 1.2 for the codrug and 130 and 20,315 days at pH 6.8 for the codrug and gemfibrozil 2-hydroxyethyl ester (GHEE), respectively. The shortest half-lives were at pH 7.4; 42 days for the codrug and 5837 days for GHEE, respectively. The hydrolysis of the latter was studied, alone, at 80°C and pH 1.2 and compared to its hydrolysis when it is produced from the codrug using similar conditions. The kobs was found in both cases to be 1.60 × 10-3 h-1. The half-lives in plasma were 35.24 min and 26.75 h for the codrug and GHEE, respectively. With regard to liver homogenate, the hydrolysis half-lives were 1.96 min and 48.13 min for the codrug and GHEE, respectively. It can be expected that in vivo, the codrug will liberate NA immediately in plasma then GEM will be liberated from its 2-hydroxyethyl ester in the liver.
Treatment of skin conditions by use of PPAR alpha activators
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Disorders of the skin and mucous membrane that have a disrupted or dysfunctional epidermal barrier are treated or prevented by topical application of compounds that are either activators of the farnesoid X receptor, activators of the peroxisome proliferator-activated receptor alpha , and oxysterol activators of the LXR alpha receptor. The same compounds are also effective in treating disorders of epidermal differentiation and proliferation.
FXR, PPARA and LXRA activators to treat acne/acneiform conditions
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Acne vulgaris and acneiform skin conditions are treated by the application of compounds that is juvenile hormone III, 7-methyl-9-(3,3-dimethyloxiranyl)-3-methyl-2,6-nonadienoic acid methyl ester.
