MW 311.33 Da, Purity >98%. Selective, non-competitive AMPA receptor antagonist. ERK1/2 pathway inhibitor. Reduces CREB phosphorylation and shows antiproliferative effects. Shows potent, long-acting anticonvulsant effects in vivo.
1,8-cineole 2-exo-monooxygenase, AI838772, AMPA 1, AMPA 3, AMPA 4, AMPA-selective glutamate receptor 1, AMPA-selective glutamate receptor 3, AMPA-selective glutamate receptor 4, AW493413, Albendazole monooxygenase, Albendazole sulfoxidase, CP33, CP34, CP3A4_HUMAN, CYP3, CYP3A, CYP3A3, CYP3A4, CYPIIIA3, CYPIIIA4, Cytochrome P450 3A3, Cytochrome P450 3A4, Cytochrome P450 HLp, Cytochrome P450 NF-25, Cytochrome P450 family 3 subfamily A polypeptide 4, Cytochrome P450 subfamily IIIA polypeptide 4, Cytochrome P450-PCN1, FLJ11090, GLUH1, GLUK3, GLUR4C, GRIA1_HUMAN, GRIA3_HUMAN, GRIA4_HUMAN, GluA 4, GluA1, GluA3, GluR-1, GluR-3, GluR-4, GluR-A, GluR-C, GluR-D, GluR-K1, GluR-K3, Glucocorticoid inducible P450, Glutamate ionotropic receptor AMPA type subunit 3, Glutamate receptor 1, Glutamate receptor 3, Glutamate receptor 4, Glutamate receptor C, Glutamate receptor ionotrophic AMPA 3, Glutamate receptor ionotrophic AMPA 4, Glutamate receptor ionotropic, Glutamate receptor ionotropic AMPA 1, Glutamate receptor subunit 3, Glutamate receptor, ionotropic, AMPA 3, HBGR1, HLP, Ionotrophic Glutamate Receptor, Ionotropic Glutamate receptor 4, MGC104252, MGC112732, MGC126680, MGC133252, MRX94, NF 25, Nifedipine oxidase, OTTHUMP00000160643, OTTHUMP00000165781, OTTHUMP00000224241, OTTHUMP00000224242, OTTHUMP00000224243, P450 III steroid inducible, P450 PCN1, P450, family III, P450C3, Quinine 3-monooxygenase, RP24-311F12.2, SCAN1, TYDP, TYDP1_HUMAN, Taurochenodeoxycholate 6-alpha-hydroxylase, Tyr-DNA phosphodiesterase 1, Tyrosyl-DNA phosphodiesterase 1, cytochrome P450, subfamily IIIA (niphedipine oxidase), polypeptide 3, cytochrome P450, subfamily IIIA (niphedipine oxidase), polypeptide 4, dJ1171F9.1
MW 311.33 Da, Purity >98%. Selective, non-competitive AMPA receptor antagonist. ERK1/2 pathway inhibitor. Reduces CREB phosphorylation and shows antiproliferative effects. Shows potent, long-acting anticonvulsant effects in vivo.
Soluble in DMSO to 100 mM.
Selective, non-competitive AMPA receptor antagonist. ERK1/2 pathway inhibitor. Reduces CREB phosphorylation and shows antiproliferative effects. Shows potent, long-acting anticonvulsant effects in vivo.
Cytochrome P450 3A4 commonly known as CYP3A4 is an enzyme with a molecular mass of about 57 kDa. It plays an important role in the metabolism of drugs in the human liver and intestine. Its expression is highest in hepatic and intestinal tissues where it catalyzes the oxidation of small organic molecules. Besides CYP3A4 modifies the chemical structure of drugs and toxins affecting their activity and clearance from the body which is important for drug interaction studies. This modification can significantly impact pharmacokinetics and pharmacodynamics.
CYP3A4 functions as part of the cytochrome P450 monooxygenase complex which helps with hormone synthesis and metabolism as well as the breakdown of various xenobiotics. It acts in cooperation with NADPH-cytochrome P450 reductase enabling electron transfer necessary for enzymatic reactions. Furthermore the enzyme shows a high degree of overlapping substrate specificity allowing it to metabolize a number of structurally diverse compounds including endogenous and exogenous substances. This flexibility highlights its essential role in hepatic detoxification processes.
CYP3A4 is integral to the drug metabolism pathway and the steroid biosynthesis pathway. It interacts with other cytochrome P450 enzymes and transport proteins such as CYP3A5 contributing to the biotransformation of drugs and natural compounds. Its function in these pathways influences the regulation of compound levels in the body impacting drug efficacy and safety. CYP3A4 activity can alter cholesterol homeostasis and the production of biochemically active steroid hormones affecting numerous physiological processes.
CYP3A4 is linked to drug-induced liver injury and cancer. Aberrant expression or mutations can lead to improper drug metabolism causing toxic accumulation and adverse drug reactions. The enzyme is often involved in the metabolic activation of procarcinogens correlating its activity with cancer risk. Additionally its interaction with P-glycoprotein influences the absorption and elimination of chemotherapeutic agents affecting treatment efficacy and patient outcomes. Understanding variations in CYP3A4 activity can aid in personalized medicine approaches to mitigate these risks.
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