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In addition, there is continuing research and development of new dual α/δ and γ/δ PPAR agonists for additional therapeutic indications, as well as "pan" agonists acting on all three isoforms. [7] [8] The anti-hypertension drug telmisartan is known to have PPAR γ/δ dual partial agonist activity in vivo. It also activates PPAR-α in vitro. [9]
This category lists drugs that act as agonists on peroxisome proliferator-activated receptors (PPARs). Subcategories This category has the following 2 subcategories, out of 2 total.
PPAR-α is primarily activated through ligand binding. Endogenous ligands include fatty acids such as arachidonic acid as well as other polyunsaturated fatty acids and various fatty acid-derived compounds such as certain members of the 15-hydroxyeicosatetraenoic acid family of arachidonic acid metabolites, e.g. 15(S)-HETE, 15(R)-HETE, and 15(S)-HpETE and 13-hydroxyoctadecadienoic acid, a ...
PPAR -alpha and -gamma pathways. In the field of molecular biology, the peroxisome proliferator–activated receptors (PPARs) are a group of nuclear receptor proteins that function as transcription factors regulating the expression of genes. [1]
It is a first in class drug which acts as a dual PPAR agonist at the subtypes α (alpha) and γ (gamma) of the peroxisome proliferator-activated receptor (PPAR). Agonist action on PPARα lowers high blood triglycerides, and agonist action on PPARγ improves insulin resistance and consequently lowers blood sugar. [2]
Fibrates, known as derivatives of fibric acids, are peroxisome proliferator-activated receptor alpha (PPAR-α) agonists primarily used for lowering TG levels and management of atherogenic dyslipidemia. [30] [31] [32] Typical drugs of the class include fenofibrate, bezafibrate, ciprofibrate and gemfibrozil.
Thiazolidinedione ligand dependent transactivation is responsible for the majority of anti-diabetic effects. The activated PPAR/RXR heterodimer binds to peroxisome proliferator hormone response elements upstream of target genes in complex with a number of coactivators such as nuclear receptor coactivator 1 and CREB binding protein, this causes upregulation of genes (for a full list see PPARγ):
A main target of PEA is proposed to be the peroxisome proliferator-activated receptor alpha (PPAR-α). [3] [4] PEA also has affinity to cannabinoid-like G-coupled receptors GPR55 and GPR119. [5] PEA cannot strictly be considered a classic endocannabinoid because it lacks affinity for the cannabinoid receptors CB1 and CB2. [6]