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phase I metabolite

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Drug Metabolite (3) 5-HT Receptor (1) Cdc42-binding kinase (1) PAK (1) Reference Standards (1) Serotonin Transporter (1)
By Research Areas:	Cancer (1) Inflammation/Immunology (1) Neurological Disease (1)

Inhibitors & Agonists

Screening Libraries

Targets Recommended: Drug Metabolite Endogenous Metabolite

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-100052

6-Hydroxybentazon 1 Publications Verification 6-Hydroxybentazone	Drug Metabolite	Others
6-Hydroxybentazon is a phase I metabolite of bentazone, and bentazone is a chemical for use in herbicides.

HY-117580

16α-Hydroxyprednisolone OH-PRED	Drug Metabolite	Inflammation/Immunology
16α-Hydroxyprednisolone (OH-PRED) is a stereoselective metabolite of the 22(R) epimer of the glucocorticoid Budesonide (HY-13580). 16α-Hydroxyprednisolone formation is catalyzed by isoenzymes within the cytochrome P450 3A (CYP3A) subfamily. 16α-Hydroxyprednisolone formation can be inhibited by antibodies targeting the CYP3A subfamily .

HY-118796

4-Hydroxy MET 4-HO-MET; 4-Hydroxy-N-methyl-N-ethyltryptamine	5-HT Receptor Serotonin Transporter	Neurological Disease
4-Hydroxy MET (4-HO-MET; 4-Hydroxy-N-methyl-N-ethyltryptamine) is a synthetic tryptamine psychoactive substance. 4-Hydroxy MET is a partial 5-HT2A receptor agonist, a serotonin transporter inhibitor and weak norepinephrine transporter inhibitor. 4-Hydroxy MET affects emotional, motoric, and cognitive functions via serotonergic hallucinogenic activity .

HY-100052R

6-Hydroxybentazon (Standard) 6-Hydroxybentazone (Standard)	Reference Standards Drug Metabolite	Others
6-Hydroxybentazon (Standard) is the analytical standard of 6-Hydroxybentazon. This product is intended for research and analytical applications. 6-Hydroxybentazon is a phase I metabolite of bentazone, and bentazone is a chemical for use in herbicides.

HY-183246

Rac/Cdc42-IN-1	PAK Cdc42-binding kinase	Cancer
Rac/Cdc42-IN-1, the major phase I metabolite of the oral Rac/Cdc42 inhibitor MBQ-167 (HY-112842) in vivo, is a selective Rac inhibitor. Rac/Cdc42-IN-1 functions by blocking the GTP-binding activation of Rac1, targeting the autophosphorylation of Thr ⁴²³/Thr ⁴⁰²/Thr ⁴³⁶ and Ser ¹⁴¹/Ser ¹⁴⁴/Ser ¹⁵⁴ in downstream PAK1/2/3, with an inhibitory effect superior to that of MBQ-167. Rac/Cdc42-IN-1 significantly inhibits cell migration, and suppresses tumor growth and distant metastasis to the lung, liver and kidney in HER2+ breast cancer mouse models. Rac/Cdc42-IN-1 can be used for targeted research on metastatic breast cancer .

Cat. No.	Product Name

HY-L076

Drug-Induced Liver Injury (DILI) Compound Library	641 compounds
Drug-induced liver injury (DILI; also known as drug-induced hepatotoxicity) is caused by medications (prescription or OTC), herbal and dietary supplements (HDS), or other xenobiotics that result in abnormalities in liver tests or in hepatic dysfunction that cannot be explained by other causes. Drugs are an important cause of liver injury. Drug-induced hepatic injury is the most common reason cited for withdrawal of an approved drug. DILI is thought to occur via several different mechanisms. Among these are direct impairment of the structural (e.g., mitochondrial dysfunction) and functional integrity of the liver; production of a metabolite that alters hepatocellular structure and function; production of a reactive drug metabolite that binds to hepatic proteins to produce new antigenic drug-protein adducts, which are targeted by hosts’ defenses (the hapten hypothesis); and initiation of a systemic hypersensitivity response (i.e., drug allergy) that damages the liver. MCE Drug-induced Liver Injury (DILI) Compound Library contains a unique collection of 641 hepatotoxicity causing compounds and is a powerful tool to research DILI and other drug toxicities. This library can be used to understand the mechanisms of DILI, identify biomarkers for early DILI prediction, and allow timely recognition during drug development, thus finally achieving successful DILI prevention and assessment in the pre-marketing phase.

Drug-Induced Liver Injury (DILI) Compound Library

641 compounds

Drug-induced liver injury (DILI; also known as drug-induced hepatotoxicity) is caused by medications (prescription or OTC), herbal and dietary supplements (HDS), or other xenobiotics that result in abnormalities in liver tests or in hepatic dysfunction that cannot be explained by other causes. Drugs are an important cause of liver injury. Drug-induced hepatic injury is the most common reason cited for withdrawal of an approved drug.

DILI is thought to occur via several different mechanisms. Among these are direct impairment of the structural (e.g., mitochondrial dysfunction) and functional integrity of the liver; production of a metabolite that alters hepatocellular structure and function; production of a reactive drug metabolite that binds to hepatic proteins to produce new antigenic drug-protein adducts, which are targeted by hosts’ defenses (the hapten hypothesis); and initiation of a systemic hypersensitivity response (i.e., drug allergy) that damages the liver.

MCE Drug-induced Liver Injury (DILI) Compound Library contains a unique collection of 641 hepatotoxicity causing compounds and is a powerful tool to research DILI and other drug toxicities. This library can be used to understand the mechanisms of DILI, identify biomarkers for early DILI prediction, and allow timely recognition during drug development, thus finally achieving successful DILI prevention and assessment in the pre-marketing phase.

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BODIPY 493/503 purchased from MedChemExpress. Usage Cited in: Nat Commun. 2025 Feb 1;16(1):1241. [Abstract]

MedchemExpress Validation 01

Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature. Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature. Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.

BODIPY 493/503 purchased from MedChemExpress. Usage Cited in: Nat Commun. 2025 Feb 1;16(1):1241. [Abstract]

MedchemExpress Validation 01

MedchemExpress Validation 03

Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred

MedchemExpress Validation 04

MedchemExpress Validation

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