this compound active metabolite

Milataxel is an orally bioavailable taxane with potential antineoplastic activity. Upon oral administration, milataxel and its major active metabolite M-10 bind to and stabilize tubulin, resulting in the inhibition of microtubule depolymerization and cell division, cell cycle arrest in the G2 M phase, and the inhibition of tumor cell proliferation. Unlike other taxane compounds, milataxel appears to be a poor substrate for the multidrug resistance (MDR) membrane-associated P-glycoprotein (P-gp) efflux pump and may be useful for treating multidrug-resistant tumors. Check for active clinical trials or closed clinical trials using this agent. (NCI Thesaurus).This compound is unstable in powder form and other related salt forms are recommended.

21-Deacetoxy deflazacort is a dehydrogenated derivative of Deflazacort, which is a glucocorticoid. As an inactive precursor, Deflazacort rapidly converts into the active metabolite, 21-Desacetyldeflazacort. This compound serves as both an anti-inflammatory and immunosuppressive agent.

22-Hydroxy Mifepristone (RU 42698) is an orally active hydroxylated alcohol metabolite that exhibits both anti-progestational and anti-glucocorticoid activities. This compound contains an alkyne group and is capable of undergoing copper-catalyzed azide-alkyne cycloaddition (CuAAC) with azide-containing molecules. Furthermore, 22-Hydroxy Mifepristone demonstrates a relative binding affinity of 48% to the human glucocorticoid receptor.

Befuraline (DIV-154) is a psychoactive compound developed in Germany during the 1970s, classified under the piperazine chemical category. This compound exhibits stimulant and antidepressant properties and has seen some application in Germany and France, although it was never widely adopted. Its active metabolite, benzylpiperazine, is primarily responsible for its effects.

O-Desmethylcarvedilol (Desmethylcarvedilol) is an active metabolite of Carvedilol, a non-selective β-adrenergic receptor (β-AR) antagonist. This compound inhibits store overload-induced calcium release in HEK293 cells expressing the RyR2 R4496C mutation (IC50= 7.62 µM). Additionally, O-Desmethylcarvedilol slows the increase in heart rate and prevents diastolic pressure reduction induced by Isoproterenol in conscious rabbits (ED50s = 32 and 5 µg kg).

cis-Clopidogrel-MP derivative, also known as Clopidogrel-MP-AM, is a 3'-methoxyacetophenone derivative of Clopidogrel active metabolite. This compound is an orally-active platelet inhibitor specifically targeting the P2Y12 receptor.

(Rac)-5-Hydroxymethyl Tolterodine hydrochloride, also known as (Rac)-Desfesoterodine hydrochloride, is an active metabolite of Tolterodine that functions as a mAChR antagonist. It exhibits significant affinity (K i values) for M1, M2, M3, M4, and M5 receptors, with values of 2.3 nM, 2 nM, 2.5 nM, 2.8 nM, and 2.9 nM, respectively. This compound is commonly employed in research related to overactive bladder conditions.

Cetirizine Impurity C dihydrochloride, a specific impurity of Cetirizine, is associated with a second-generation antihistamine that serves as the carboxylated metabolite of hydroxyzine. This compound acts as a specific, orally active, and long-acting antagonist of the histamine H1-receptor [1] [2].

Roxatidine, the active metabolite of Roxatidine acetate hydrochloride, serves as a histamine H2-receptor antagonist and exhibits anti-ulcer properties. It functions by suppressing the release of histamine, thereby inhibiting proton secretion, and also reduces the production of VEGF-1, a key indicator of inflammation and angiogenesis. This compound demonstrates an anti-allergic inflammatory effect [1].

2,3-Dinor-8-iso Prostaglandin F1α (2,3-dinor-8-iso PGF1α), an isoprostane and active metabolite of arachidonic acid deriving its formation from non-enzymatic free radical peroxidation, acts as an active metabolite of the platelet aggregation inhibitor 8-iso PGF2α. This compound exhibits vasoconstrictive properties in isolated porcine retinal and brain microvessels with EC50 values of 12.8 and 18.5 nM, respectively, yet it does not cause contraction in isolated rat aortic rings at a concentration of 31 µM. Further, at a concentration of 1 µM, it raises thromboxane B2 (TXB2) levels in isolated porcine brain slices, an effect reversible by thromboxane A synthase inhibitor CGS 12970, voltage-gated calcium channel inhibitor SKF 96365, or the nicotinic acetylcholine receptor (nAChR) antagonist α-conotoxin.

Tauro-obeticholic acid, a farnesoid X receptor (FXR) agonist and semisynthetic derivative of chenodeoxycholic acid, is an active metabolite of obeticholic acid. This compound undergoes taurine conjugation in the liver to form from obeticholic acid and can be reconverted to its original form by intestinal microflora.

5α-Pregnane-3α,20α-diol, an active metabolite of progesterone, is synthesized through intermediates 5α-pregnane-20α-ol-3-one and 5α-pregnane-3α-ol-20-one from progesterone. This compound, at a concentration of 10 µM, elevates intracellular calcium levels in washed isolated human platelets.

Dabigatran acyl-β-D-glucuronide, an active metabolite of the thrombin inhibitor dabigatran, is synthesized predominantly through the action of the UDP-glucuronosyltransferase isoform UGT2B15. This compound, at a concentration of 0.46 µM, effectively prolongs activated partial thromboplastin time (aPTT) in isolated human platelet-poor plasma.

(S)-5-hydroxy-6-methoxy Duloxetine, an active metabolite of the (S)-duloxetine, functions as a serotonin (5-HT) and norepinephrine reuptake inhibitor. Its formation occurs through the cytochrome P450 (CYP) isoforms CYP1A2 and CYP2D6 via a 5- or 6-hydroxy duloxetine intermediate, followed by a catechol duloxetine intermediate. This compound effectively inhibits the serotonin transporter (SERT), norepinephrine transporter (NET), and dopamine transporter (DAT) across lipid membranes, with inhibition constants (Kis) of 266, 920, and 2,814 nM, respectively, for human transporters.

S-(N-Methylsulfinylbutylthiocarbamoyl)-L-cysteine (SFN-Cys) is an isothiocyanate derivative, functioning as an active metabolite of sulforaphane, a class I and II histone deacetylase (HDAC) inhibitor, and anticancer agent. This compound is generated from sulforaphane through intermediates - DL-sulforaphane glutathione and sulforaphane cysteinylglycine - via the mercapturic acid pathway enzymes. At a concentration of 20 µM, SFN-Cys diminishes invasion and migration of U87MG and U373 MG glioblastoma cells as observed in wound healing and chamber assays. Furthermore, at 45 µM, it significantly lowers the expression of α-tubulin, βIII-tubulin, stathmin 1, and X-linked inhibitor of apoptosis (XIAP), and also reduces cell density in paclitaxel-resistant A549 lung cancer cells (A549/T). Additionally, when used at 30 µM, SFN-Cys prompts apoptosis and cell cycle arrest at the G2/M phase in U87MG and U373 MG cells.

6-Hydroxy Buspirone, an active metabolite of the anxiolytic compound buspirone, is produced via the cytochrome P450 (CYP) isoform CYP3A4. This compound exhibits affinity for the serotonin (5-HT) receptor subtype 5-HT1A, demonstrating efficacy in the rat hippocampus and dorsal raphe with half-maximal effective concentrations (EC50s) of 4 and 1 µM, respectively. Furthermore, 6-Hydroxy Buspirone acts as a potent antagonist against dopamine D2, D3, and D4 receptors with half-maximal inhibitory concentrations (IC50s) of 3.1, 4.9, and 0.85 µM, respectively, and inhibits the organic cation transporters 1 (OCT1), OCT2, and OCT3 in S2 proximal tubule cells expressing human transporters, showcasing a concentration-dependent mechanism.

Vinclozolin M2, an active metabolite of vinclozolin, is generated through successive esterase activity and decarboxylation in C. elegans, as well as decarboxylation in human liver microsomes. It functions as an antagonist to the mineralocorticoid (IC50= 1,400 nM) and androgen receptors (IC50= 0.17 nM), demonstrated in reporter assays with MCF-7 cells. This compound is exclusively sold for research and analytical purposes, tailored for controlled laboratory use, and is not available in bulk sizes.

5(S)-HEPE, an active metabolite of eicosapentaenoic acid (EPA), is produced via the action of 5-lipoxygenase (5-LO). This compound functions as an agonist for G protein-coupled receptor 119 (GPR119), promoting cAMP accumulation in CHO-K1 cells expressing human GPR119 at 10 µM concentration. Additionally, 5(S)-HEPE enhances glucose-stimulated insulin secretion from MING6 insulinoma pancreatic islets and glucagon-like peptide 1 (GLP-1) secretion from HuTu 80 adenocarcinoma cells at the same concentration. Notably, serum levels of 5(S)-HEPE are increased in hyperlipidemia patients.

Desethoxy quetiapine, an active metabolite of the atypical antipsychotic quetiapine, primarily forms through the action of the cytochrome P450 (CYP) isoform CYP3A5. This compound binds to dopamine D2 receptors with an IC50 value of 1,330 nM. In vivo, desethoxy quetiapine at dosages of 20 and 40 mg kg mitigates dopamine receptor agonist apomorphine-induced climbing behavior and ameliorates swimming deficits in mice, showcasing its potential modulatory effects on dopamine-mediated behaviors.

N-Desmethyl Regorafenib N-oxide, an active metabolite of the multi-kinase inhibitor regorafenib, originates through the action of the cytochrome P450 (CYP) isoform CYP3A4. This compound demonstrates efficacy in vitro by inhibiting key enzymes such as VEGFR2, Tie2, c-Kit, and B-RAF, and it exhibits tumor growth inhibition in HT-29 and MDA-MB-231 mouse xenograft models at a dosage of 1 mg/kg.

Trans-Resveratrol-3-O-β-D-Glucuronide, an active metabolite of trans-resveratrol, inhibits the proliferation of various intestinal cancer cell lines. Additionally, this compound enhances pyruvate production in the liver [1] [2] [3].

Sulindac-d3 is a deuterated compound of Sulindac. Sulindac has a CAS number of 38194-50-2. Sulindac is a sulfinylindene derivative prodrug with potential antineoplastic activity. Converted in vivo to an active metabolite, sulindac, a nonsteroidal anti-inflammatory drug (NSAID), blocks cyclic guanosine monophosphate-phosphodiesterase (cGMP-PDE), an enzyme that inhibits the normal apoptosis signal pathway; this inhibition permits the apoptotic signal pathway to proceed unopposed, resulting in apoptotic cell death.