39 results about "Peroxisome Proliferation" patented technology

The invention relates to the discovery that farnesoid X receptor (FXR) agonists can be used in combination with peroxisome proliferation activated receptor gamma (PPARγ) agonists to reduce drug-induced adverse side effects in patients suffering from conditions such as insulin resistance, Type II diabetes, metabolic syndrome, non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), and heart disease. Particularly, the present invention encompasses methods for treating patients suffering from drug-induced adverse side effects with selective PPARγ, dual PPARα/γ and pan PPARα/γ/δ agonists in combination with FXR agonists.

A compound represented by the general formula (II) below or a salt thereof is used as an activating agent for PPAR d. (II) (In the formula, G represents O, CH2 or the like; A represents a thiazole, oxazole or thiophene which may have a substituent selected from an alkyl group having 1-8 carbon atoms, an alkoxy group having 1-8 carbon atoms, a halogen atom, an alkyl group having 1-8 carbon atoms and substituted by a halogen atom and the like; B represents an alkylene chain having 1-8 carbon atoms, and when the alkylene chain has two or more carbon atoms, it may have a double bond; and R<1a> and R<2a> respectively represent a hydrogen atom, an alkyl group having 1-8 carbon atoms, an alkoxy group having 1-8 carbon atoms, a halogen atom, an alkyl group having 1-8 carbon atoms and substituted by a halogen atom or the like.

The invention provides novel substituted phenylpropanoic acid derivatives that activate by binding to receptor as ligands of human peroxisome preliferant-activated receptor alpha (PPARalpha), and exhibit potent decreasing action on lipids in blood (cholesterol and triglyceride).It relates to a substituted phenylpropanoic acid derivatives represented by a general formula (1),their pharmaceutically acceptable salts and their hydrates, and processes for preparing them.

Disorders of the skin and mucous membranes 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.

The present invention is directed to compounds of the structural Formula: wherein: R¹ is H or —C₁-C₃ alkyl; R² is selected from the group consisting of —H, —C₁-C₄ alkyl, —C₁-C₃ alkyl-CF₃, phenyl, and pyridinyl; and R³ is selected from the group consisting of —H, —C₁-C₄ alkyl, —C₁-C₃ alkyl-O—CH₃, —CH₂-cyclopropyl, CH₂—C═CH₂, —CH₂CH₂-(2-F-phenyl), and phenyl substituted with from 1 to 2 fluorines; provided that when R¹ and R² are each H, then R³ is selected from the group consisting of —C₁-C₄ alkyl, —C₁-C₃ alkyl-O—CH₃, —CH₂-cyclopropyl, —CH₂—C═CH₂, —CH₂CH₂-(2-F-phenyl), and phenyl substituted with from 1 to 2 fluorines; or stereoisomers and pharmaceutically acceptable salts thereof.

The invention relates to a PPAR (Peroxisome Proliferator-Activated Receptor) alpha gene and application thereof as goose fat traits genetic markers. Genetic markers related to abdomen fat weight and abdomen fat ratio in the PPAR alpha gene are measured; the existence of polymorphism in the PPAR alpha gene in a nucleic acid sample obtained from a goose is measured, wherein the polymorphism is related to the abdomen fat weight and the abdomen fat ratio; and the fat traits selection breeding can be carried out on the goose containing the PPAR alpha gene in a genome DNA according to the single nucleotide polymorphism of the gene, and an advantageous genotype for reducing the abdomen fat weight and the abdomen fat ratio is obtained by the screening. The invention has extremely important application value and economic benefit.

The present invention relates to the use of a pharmaceutical composition in the form of extended-release tablets containing Pirfenidone for treating NAFLD/NASH and advanced liver fibrosis by decreased serum cholesterol and triglycerides as well as reducing the content of hepatic fat accumulation, both in the form of macrosteatosis and microsteatosis. Additionally, its use as an agonist for PPARgamma (peroxisome proliferation receptor activated gamma), PPARalpha (peroxisome proliferation receptor activated alpha), LXR and CPT1, key molecules in the metabolism of fatty degradation and inflammation of the liver. In addition, another use is the induction of decreased expression of NFkB master gene, transcriptional inducer of hepatic inflammatory process factor. All of these events results in the reversal of NAFLD/NASH and advanced liver fibrosis.

The present invention is directed to compounds represented by the following structural formula, and pharmaceutically acceptable salts thereof, Formula I. (Formula I); wherein: (a) R5 is selected from the group consisting of (C₁-C₆) alkyl, (C₁-C₆) alkenyl, aryl (C₀-C₄) alkyl, aryloxy (C₀-C₄) alkyl, arylthio (C₀-C₄) alkyl, and further wherein when R5 is alkyl, R5 can optionally combine with W to form a 6 membered cycloheteroalkyl ring that is fused with the oxazole or thiazole ring to which the R5 group is attached; (b) R9 is selected from the group consisting of C₁-C₅ alkyl, C₁-C₅ alkenyl, and arylC₀-C₃alkyl. (c) T₁ is selected from the group consisting of C and N, (d) W is selected from the group consisting of CH₂, C(O)N(R21), N(R21), N(R21)CH₂, O, OCH₂, S, and SO₂; and (e) X is selected from the group consisting of C, CH₂C, and CCH₂

Method of treating diseases associated with peroxisome proliferator-activated receptors by administering to a subject in need thereof an effective amount of 15-ketoprostaglandin-delta ¹³ - Reductase modulators. Also disclosed is a method of identifying a compound that inhibits the reductase activity, and a method of lowering blood glucose levels by administering to a subject an effective amount of the reductase inhibitor.

The present invention is directed to compounds represented by the following structural formula, and pharmaceutically acceptable salts, solvates and hydrates thereof, R1 is a substituted or unsubstituted group selected from C₁-C₈ alkyl, aryl-C_0-2-alkyl, heteroaryl-C_0-2-alkyl, C₃-C₆ cycloalkylaryl-C_0-2-alkyl or phenyl. W is O or S. R2 is H or a substituted or unsubstituted group selected from C₁-C₆ alkyl, C₃-C₆ cycloalkyl and heteroaryl. X is a C₂-C₅ alkylene linker wherein one carbon atom of the linker may be replaced with O, NH or S. Y is C, O, S, NH or a single bond. Furthermore, E is (CH₂)_nCOOH, wherein n is 0, 1, 2 or 3, or C(R3)(R4)A, wherein A is an acidic functional group such as carboxyl, carboxamide substituted or unsubstituted sulfonamide, or substituted or unsubstituted tetrazole. R3 is H, saturated or unsaturated C₁-C₅ alkyl, C₁-C₅ alkoxy. Additionally, R4 is H, halo, a substituted or unsubstituted group selected from C₁-C₅ alkyl, C₁-C₅ alkoxy, C₃-C₆ cycloalkyl, arylC₀-C₄alkyl and phenyl, or R3 and R4 are combined to form a C₃-C₄ cycloalkyl.

The present invention is directed to compounds represented by the following structural formula, and pharmaceutically acceptable salts thereof, Formula I: wherein: (a) R5 is selected from the group consisting of (C₁-C₆) alkyl, (C₁-C₆) alkenyl, substituted aryl(C₀-C₄)alkyl, substituted aryloxy(C₀-C₄)alkyl, substituted arylthio(C₀-C₄)alkyl, unsubstituted aryl(C₀-C₄)alkyl, unsubstituted aryloxy(C₀-C₄)alkyl, and unsubstituted arylthio(C₀-C₄)alkyl; (b) T1 is C or N; (c) Q is selected from the group consisting of O, a single bond, O(CH₂)_q and C; (d) q is 1 or 2; (e) W is selected from the group consisting of O, S, (CH₂)_rN(R20)(CH₂)_k, NHSO₂, C(O)N(R20)(CH₂)_r, (CH₂)_rN(R20)C(O), and SO₂; (f) X is C_mH_2m; (g) m is 0, 1 or 2; (h) A is an functional group selected from the group consisting of carboxyl, C1-C3 alkylnitrile, carboxamide, and (CH₂)_nCOOR19; and (i) R19 is selected from the group consisting of hydrogen, optionally substituted C1-C4alkyl and optionally substituted arylmethyl.

A detection method for detecting adipogenic potential of mesenchymal stem cells comprises the following steps: respectively collecting d0 cells and d7 cells, and respectively extracting total RNA of the d0 cells and the d7 cells; synthesizing cDNA from the total RNA of the d0 cell and the d7 cell respectively; and detecting and calculating the relative expression quantity of the peroxisome proliferative activation receptor gamma 2 of the d0 cells and d7 cells by taking peroxisome proliferative activation receptor gamma 2 as a primer and 18S rRNA as an internal reference, and judging that the mesenchymal stem cells have the large adipogenesis potential when the ratio of X7:X0 is larger than or equal to 10. The detection method for detecting the adipogenesis potential of the mesenchymal stemcells can judge that whether the mesenchymal stem cells have large adipogenesis potential or not by detecting the relative expression quantity of the peroxisome proliferative activation receptor gamma 2 on the seventh day of induction, so the detection method has great significance in the adipogenesis induction culture process of the mesenchymal stem cells.

The invention belongs to the field of medicinal chemistry and provides an application of ciglitazone in preparing drugs for treating pulmonary arterial hypertension. An experiment of the invention proves that ciglitazone is capable of effectively reducing average pulmonary artery pressure and pulmonary vasculature resistance of pulmonary arterial hypertension rats, increasing cardiac output, reducing right ventricular hypertrophy index, improving pulmonary vasculature remodeling and increasing protein expression of Gamma(peroxisome proliferation activated receptor, PPAR Gamma). The experimentproves that ciglitazone has a therapeutic effect on pulmonary arterial hypertension.