p450s

S-(p-Nitrobenzyl)glutathione acts as a competitive inhibitor of glutathionase. Rat kidney microsomes convert this compound into associated cysteine derivatives. It serves as a research tool in investigating the catabolism of glutathione by the glutathionase system [1] [2].

(S,E)-2-Methyl-6-(p-tolyl)hept-3-en-2-ol is a useful organic compound for research related to life sciences and the catalog number is T125520.

Super-chelating agent & MRI contrast agent

Compound 40, NH2-c[X-R-L-S-X]-K-G-P-(D-2Nal), a macrocyclic analogue of Ape13, acts as a potent APJ agonist with a Ki of 5.7 nM. It demonstrates favorable Gα12-biased signaling and possesses an enhanced in vivo half-life [1].

Compound 39 (NH2-c[X-R-L-S-X]-K-G-P-(D-1Nal)) is a potent agonist of the APJ receptor, possessing a K i value of 0.6 nM. It is capable of activating Gαi1, with an EC 50 of 0.8 nM, and of recruiting β-arrestin2, with an EC 50 of 31 nM. Furthermore, this compound demonstrates extended effects on cardiac function [1].

Piperonylic acid (2H-1,3-benzodioxole-5-carboxylic acid) is a natural molecule bearing a methylenedioxy function that closely mimics the structure of trans-cinnamic acid. Piperonylic acid selectively inactivate the CYP73A P450 subpopulation.

7ETMC is a selective Human Cytochrome P450s 1A1 and 1A2 inhibitor. 7ETMC showed IC50s of 0.46 μM and 0.50 μM for P450s 1A1 and 1A2 in the first six minutes, respectively, and did not show any inhibition activity for P450s 2A6 and 2B1 even at the dose of 5

7α-hydroxy Dehydroepiandrosterone (7α-hydroxy DHEA) is an active metabolite of the endogenous steroid hormone dehydroepiandrosterone .17α-hydroxy DHEA is formed from dehydroepiandrosteronevia7-hydroxylation by cytochrome P450s (CYPs).2It increases antigen-induced production of anti-tetanus toxoid and anti-pertussis antigen IgGs in co-cultures of human tonsil-derived B and T cells when used at a concentration of 1 μM.37α-hydroxy DHEA (6.25 mg/kg) increases serum concentrations of anti-lysozyme IgG in mice.1

N-Desbutyl dronedarone is an active metabolite of the antiarrhythmic agent dronedarone .1,2,3It is formed from dronedarone by cytochrome P450s (CYPs) and monoamine oxidase (MAO) in human hepatocyte preparations.4N-Desbutyl dronedarone inhibits the binding of 3,3’,5-triiodo-L-thyronine to the thyroid hormone receptors TRα1and TRβ1(IC50s = 59 and 280 μM for the chicken and human receptors, respectively).1It inhibits CYP2J2-mediated formation of 14,15-EET from arachidonic acid and soluble epoxide hydrolase-mediated formation of 14,15-DHET from 14,15-EET (IC50s = 1.59 and 2.73 μM, respectively, in cell-free assays).2N-Desbutyl dronedarone decreases intracellular ATP levels in H9c2 rat cardiomyocytes (IC50= 1.07 μM) and inhibits mitochondrial complex I, also known as NADH dehydrogenase, and mitochondrial complex II, also known as succinate dehydrogenase, activities in isolated rat heart mitochondria (IC50s = 11.94 and 24.54 μM, respectively).3 1.Van Beeren, H.C., Jong, W.M.C., Kaptein, E., et al.Dronerarone acts as a selective inhibitor of 3,5,3’-triiodothyronine binding to thyroid hormone receptor-α1: in vitro and in vivo evidenceEndocrinology144(2)552-558(2003) 2.Karkhanis, A., Tram, N.D.T., and Chan, E.C.Y.Effects of dronedarone, amiodarone and their active metabolites on sequential metabolism of arachidonic acid to epoxyeicosatrienoic and dihydroxyeicosatrienoic acidsBiochem. Pharmacol.146188-198(2017) 3.Karkhanis, A., Leow, J.W.H., Hagen, T., et al.Dronedarone-induced cardiac mitochondrial dysfunction and its mitigation by epoxyeicosatrienoic acidsToxicol. Sci.163(1)79-91(2018) 4.Klieber, S., Arabeyre-Fabre, C., Moliner, P., et al.Identification of metabolic pathways and enzyme systems involved in the in vitro human hepatic metabolism of dronedarone, a potent new oral antiarrhythmic drugPharmacol. Res. Perspec.2(3)e00044(2014)

1. Acetylshikonin exhibits weak cytotoxicity against human umbilical vein endothelial cells (HUVECs) with IC5 of over 2 microM, exhibits the antiangiogenic and antitumorigenic effects by suppressing proliferation and angiogenic factors. 2. Acetylshikonin inhibits the generation of NADPH oxidase complex in the activation of respiratory burst of PMNs, but does not directly inhibit the activity of NADPH oxidase already generated. 3. Certain shikonin derivatives(such as Acetylshikonin) act as modulators of the Nur77-mediated apoptotic pathway and identify a new shikonin-based lead that targets Nur77 for apoptosis induction. 4. Acetylshikonin, shikonin, and alkannin have accelerative effect on the proliferation of granulation tissue in rats. 5. Acetylshikonin has inhibitory effect on the edematous response is due neither to the release of steroid hormones from the adrenal gland nor to the glucocorticoid activity, but probably partly to the suppression of mast cell degranulation and partly to protection of the vasculature from mediator challenge. 6. Acetylshikonin induces apoptosis of hepatitis B virus X protein-expressing human hepatocellular carcinoma cells via endoplasmic reticulum stress.