Prediction

By Targets:	Amylases (1) Carbonic Anhydrase (1) Drug Metabolite (1) EGFR (2) Endogenous Metabolite (3) Fungal (1) Glucosidase (1) IRAK (1) Monoamine Oxidase (1) P-glycoprotein (1) SARS-CoV (1)
By Research Areas:	Cancer (3) Infection (2) Inflammation/Immunology (1) Metabolic Disease (2) Neurological Disease (2)

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-100978

(±)-Hexanoylcarnitine chloride DL-Hexanoylcarnitine chloride	Endogenous Metabolite	Metabolic Disease
(±)-Hexanoylcarnitine chloride is a fatty acid metabolite that breaks down fatty acids into energy that can be used by the body. (±)-Hexanoylcarnitine chloride also serves as a specific and easily detectable biomarker for rat skeletal muscle toxicity. Cerivastatin (HY-129458) and TMPD (HY-W012145) induce an increase in Hexanoylcarnitine in rats in a metabolomic analysis of the rectus femoris muscle. In type 2 diabetes, Hexanoylcarnitine is also significantly associated with and improves prediction of all-cause mortality. Hexanoylcarnitine is a biomarker for the identification of novel pathogenic pathways .

HY-163380

CA/MAO-B-IN-1	Carbonic Anhydrase	Neurological Disease
CA/MAO-B-IN-1 (Compound 78) is a dual inhibitor for human brain carbonic anhydrases (CA) and Monoamine Oxidase-B (MAO-B), with IC₅₀s of 8.8 and 7.0 nM, respectively. CA/MAO-B-IN-1 reveals a human oral absorption of 71.9% through in silico prediction .

HY-113157

Estrone 3-glucuronide	Drug Metabolite Endogenous Metabolite	Others
Estrone 3-glucuronide is deuterium labeled Estrone 3-glucuronide. Estrone 3-glucuronide, the dominant metabolite of estradiol, is determined to be the urinary marker for prediction of the fertile window .

HY-163415

MAO-IN-5	Monoamine Oxidase	Neurological Disease
MAO-IN-5 (Compound ZINC000016952895) is a monoamine oxidase (MAO) inhibitor. According to the prediction of Swiss ADME, MAO-IN-5 can inhibit the CYP enzyme family, has blood-brain barrier (BBB) permeability, and has a high gastrointestinal absorption rate. MAO-IN-5 can be used in the study of neurological diseases .

HY-146113

IRAK4-IN-15	IRAK	Cancer
IRAK4-IN-15 (compound 35) is a potent and selective IRAK4 inhibitor with an IC₅₀ of 0.002 µM. IRAK4-IN-15 shows good human PK predictions with low intrinsic clearance. IRAK4-IN-15 shows great synergistic in vitro activity against MyD88/CD79 double mutant ABC-DLBCL in combination with Acalabrutinib. .

HY-155416

M56-S2 iodide	SARS-CoV	Infection
M56-S2 iodide is a SARS-CoV-2 M ^pro inhibitor (IC₅₀=4.0 μM). M56-S2 iodide showed good oral bioavailability and low toxicity in ADMET prediction. M56-S2 iodide has good drug potential and can be used in antiviral (such as SARS-CoV-2) research .

HY-113111

11,12-DiHETrE	Endogenous Metabolite	Inflammation/Immunology
11,12-DiHETrE, an endogenous metabolite, is a Cytochrome P450 (P450) eicosanoid. 11,12-DiHETrE can be used for preterm labor research. 11,12-DiHETrE can be used as a single biomarker for differentiating NAFL (nonalcoholic fatty liver) from NASH (nonalcoholic steatohepatitis) .

HY-147919

Antifungal agent 33	Fungal	Infection
Antifungal agent 33 (compound 4e) is a potent antifungal agent. Antifungal agent 33 exhibits remarkable antifungal activity against C. albicans, with a MIC of 16 μg/mL. Antifungal agent 33 shows potent inhibitory activity against Lanosterol 14α-demethylase (CYP51), with an IC₅₀ of 0.19 μg/mL .

HY-151158

EGFR/HER2-IN-7	EGFR	Cancer
EGFR/HER2-IN-7 is a potent anticancer agent with high selectivity against MCF-7 breast cancer cells. EGFR/HER2-IN-7 is a EGFR/HER2 kinase and DHFR inhibitor, with IC₅₀s of 0.18 μM (EGFR), 0.146 μM (HER2), respectively. EGFR/HER2-IN-7 shows moderate inhibition on DHFR (IC₅₀=0.907 μM) .

HY-151154

EGFR/HER2/DHFR-IN-1	EGFR	Cancer
EGFR/HER2/DHFR-IN-1 is a potent anticancer agent with high selectivity against MCF-7 breast cancer cells. EGFR/HER2/DHFR-IN-1 is a multiple inhibitor of EGFR/HER2 kinase and DHFR, with IC₅₀s of 0.153 μM, 0.108 μM, 0.291 μM, respectively. EGFR/HER2/DHFR-IN-1 arrests cell cycle at G1/S and induces cells apoptosis .

HY-162373

α-Amylase/α-Glucosidase-IN-10	Amylases Glucosidase P-glycoprotein	Metabolic Disease
α-Amylase/α-Glucosidase-IN-10 (compound 5d) is an α-amylase and α-glucosidase inhibitor (IC₅₀: 30.39 μM and 65.1 μM) with potential diabetes inhibitory effects. α-Amylase/α-Glucosidase-IN-10 exhibits high gastrointestinal (GI) absorption in ADMET (Absorption, Distribution, Metabolism, Excretion and Toxicity) prediction. While α-Amylase/α-Glucosidase-IN-10 acts as a substrate for P-gp and does not cross the blood-brain barrier (BBB), there may be a risk of central nervous system side effects .

Cat. No.	Product Name

HY-L076

Drug-Induced Liver Injury (DILI) Compound Library	1,392 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 1,392 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

1,392 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 1,392 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.

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-100978

(±)-Hexanoylcarnitine chloride DL-Hexanoylcarnitine chloride	Structural Classification Classification of Application Fields Ketones, Aldehydes, Acids Source classification Metabolic Disease Endogenous metabolite Disease Research Fields	Endogenous Metabolite
(±)-Hexanoylcarnitine chloride is a fatty acid metabolite that breaks down fatty acids into energy that can be used by the body. (±)-Hexanoylcarnitine chloride also serves as a specific and easily detectable biomarker for rat skeletal muscle toxicity. Cerivastatin (HY-129458) and TMPD (HY-W012145) induce an increase in Hexanoylcarnitine in rats in a metabolomic analysis of the rectus femoris muscle. In type 2 diabetes, Hexanoylcarnitine is also significantly associated with and improves prediction of all-cause mortality. Hexanoylcarnitine is a biomarker for the identification of novel pathogenic pathways .

HY-113157

Estrone 3-glucuronide	Structural Classification Classification of Application Fields Source classification Other Diseases Endogenous metabolite Disease Research Fields Steroids	Drug Metabolite Endogenous Metabolite
Estrone 3-glucuronide is deuterium labeled Estrone 3-glucuronide. Estrone 3-glucuronide, the dominant metabolite of estradiol, is determined to be the urinary marker for prediction of the fertile window .

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