Compound Information | SONAR Target prediction |
Name: | Fenofibrate |
Unique Identifier: | Prest217 |
MolClass: | Checkout models in ver1.5 and ver1.0 |
Molecular Formula: | C20ClH21O4 |
Molecular Weight: | 339.664 g/mol |
X log p: | 16.598 (online calculus) |
Lipinksi Failures | 1 |
TPSA | 52.6 |
Hydrogen Bond Donor Count: | 0 |
Hydrogen Bond Acceptors Count: | 4 |
Rotatable Bond Count: | 7 |
Canonical Smiles: | CC(C)OC(=O)C(C)(C)Oc1ccc(cc1)C(=O)c1ccc(Cl)cc1 |
Generic_name: | Fenofibrate |
Chemical_iupac_name: | 1-methylethyl2-[4-(4-chlorobenzoyl)phenoxy]-2-methyl-propanoate |
Drug_type: | Approved Drug |
Pharmgkb_id: | PA449594 |
Kegg_compound_id: | C07586 |
Drugbank_id: | APRD00405 |
Melting_point: | 80.5 ᄚC |
H2o_solubility: | 0.25mg/ml at 25 ᄚC |
Logp: | 5.575 |
Cas_registry_number: | 49562-28-9 |
Drug_category: | Antilipemic Agents; Fribic Acid Derivatives; ATC:C10AB05 |
Indication: | For use as adjunctive therapy to diet to reduce elevated LDL-C, Total-C,Triglycerides and Apo B, and to increase HDL-C in adult patients with primary hypercholesterolemia or mixed dyslipidemia (Fredrickson Types IIa and IIb) |
Pharmacology: | Fenofibrate is a lipid regulating agent indicated as adjunctive therapy to diet to reduce elevated LDL-C, Total-C,Triglycerides and Apo B, and to increase HDL-C in adult patients with primary hypercholesterolemia or mixed dyslipidemia (Fredrickson Types IIa and IIb). Fenofibrate is also indicated as adjunctive therapy to diet for treatment of adult patients with hypertriglyceridemia (Fredrickson Types IV and V hyperlipidemia). Fenofibric acid, the active metabolite of Fenofibrate, produces reductions in total cholesterol, LDL cholesterol, apolipoprotein B, total triglycerides and triglyceride rich lipoprotein (VLDL) in treated patients. In addition, treatment with fenofibrate results in increases in high density lipoprotein (HDL) and apoproteins apoAI and apoAII. |
Mechanism_of_action: | Fenofibrate exerts its therapeutic effects through activation of peroxisome proliferator activated receptor a (PPARa). This increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III. The resulting fall in triglycerides produces an alteration in the size and composition of LDL from small, dense particles, to large buoyant particles. These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly. |
Organisms_affected: | Humans and other mammals |