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Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
55 Results for "
hepatic dysfunction
" in MedChemExpress (MCE) Product Catalog:
Products (55)
55 Results for "hepatic dysfunction" in MCE Product Catalog:
Cat. No.: HY-187385
Target:
Research Areas:
GPR35 agonist 8 is a cross-species, highly potent GPR35 agonist (human EC50: 12 nM; murine EC50: 2 nM). GPR35 agonist 8 reduces lipid accumulation, ameliorates lipid metabolism disorders, alleviates hepatic inflammation and liver fibrosis, and relieves hepatic steatosis. GPR35 agonist 8 can be used for research on metabolic dysfunction-associated fatty liver disease and metabolic dysfunction-associated steatohepatitis .
Cat. No.: HY-187384
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GPR35 agonist 7 is a selective GPR35 agonist, with an EC50 of 0.030 μM for hGPR35 and an EC50 of 0.021 μM for mGPR35. GPR35 agonist 7 reduces lipid accumulation. In a high-fat diet-induced MASH mouse model, GPR35 agonist 7 improves hepatic steatosis, corrects lipid metabolism disorders, alleviates hepatic inflammation and attenuates hepatic fibrosis. GPR35 agonist 7 can be used for the research of metabolic dysfunction-associated steatohepatitis .
Cat. No.: HY-182751
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ACLY-IN-4 is an ATP-citrate lyase (ACLY) inhibitor with an IC50 of 0.022 μM and a Kd of 0.19 μM. ACLY-IN-4 binds to the allosteric binding site of ACLY. ACLY-IN-4 exhibits hypolipidemic, anti-steatotic, insulin sensitivity-improving, anti-oxidative stress, anti-inflammatory and anti-fibrotic activities. ACLY-IN-4 alleviates hepatic steatosis, systemic insulin resistance, oxidative stress, hepatic inflammation and fibrosis. ACLY-IN-4 can be used for the research of metabolic dysfunction-associated steatohepatitis .
Cat. No.: HY-L076
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.
Cat. No.: HY-182750
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ACLY-IN-3 is an ATP-citrate lyase (ACLY) inhibitor with an IC50 of 0.036 μM and a target Kd of 0.54 μM. ACLY-IN-3 interacts with the allosteric binding site of ACLY to inhibit its activity. ACLY-IN-3 exhibits excellent lipid-lowering effects and alleviates hepatic inflammation and liver fibrosis. ACLY-IN-3 can be used for the research of metabolic dysfunction-associated steatohepatitis .
Cat. No.: HY-N17383
CAS No.: 2283387-37-9
Cat. No.: HY-153149
CAS No.: 945457-84-1
Synonyms: FM101
Research Areas:
LJ-2698 (FM101) is an orally active adenosine A3 receptor (Adenosine A3 Receptor) antagonist . LJ-2698 blocks adenosine A3 receptor-dependent pro-inflammatory JNK, ERK, and NF-κB signaling pathways. LJ-2698 prevents alveolar cavity enlargement, restores pulmonary function, and inhibits matrix metalloproteinase activity and pulmonary cell apoptosis (apoptosis) in mice . LJ-2698 induces mitochondrial dysfunction, necroptosis, and intrinsic apoptosis. LJ-2698 ameliorates renal injury in mice with diabetic nephropathy, and alleviates diet-induced hepatic inflammation and fibrosis. LJ-2698 can be used in the research of emphysema, diabetic nephropathy, and metabolic dysfunction-associated steatotic liver disease .
Cat. No.: HY-183279
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FXR antagonist 4 (Compound 4l) is an orally active, selective FXR antagonist with an IC50 of 0.70 μM. FXR antagonist 4 binds to FXR, differentially regulates bile acid and lipid transporter genes, and exerts no effect on gluconeogenesis-related genes. FXR modulator 1 activates the AMPK signaling pathway to inhibit fatty acid synthesis. FXR modulator 1 alleviates hepatic steatosis, ballooning degeneration and fibrosis, and improves dyslipidemia. FXR modulator 1 can be used for research on metabolic dysfunction-associated steatohepatitis .
Cat. No.: HY-187505
CAS No.: 3052796-86-5
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ZG-2585 is an orally active and selective thyroid hormone receptor β (THRβ) agonist. ZG-2585 selectively activates THRβ over THRα, driving allosteric conformational changes and coactivator recruitment. ZG-2585 reduces body weight, hepatic steatosis and lipid accumulation in a Western diet-induced metabolic disorder model. ZG-2585 can be used for the research of metabolic disorders, including obesity, dyslipidemia and metabolic dysfunction-associated steatohepatitis .
Cat. No.: HY-184312
CAS No.: 1031072-40-8
Research Areas:
PPAR agonist 8 is an orally active pan-PPAR agonist, with KD values of 0.576 μM, 2.06 μM and 1.45 μM for PPARα, PPARγ and PPARδ, respectively. PPAR agonist 8 upregulates the expression of ATP-binding cassette transporter A1 (ABCA1) and promotes cholesterol efflux. PPAR agonist 8 reduces plasma cholesterol levels, decreases cholesterol accumulation in the liver and cholesterol deposition in pancreatic islets, regulates glucose and lipid metabolism, and causes no side effects of weight gain and obesity. PPAR agonist 8 can be used in the research of type 2 diabetes, hepatic steatosis and pancreatic islet dysfunction .
Cat. No.: HY-182294
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HYJ-2 is a URAT1 inhibitor and urate-lowering agent. HYJ-2 inhibits URAT1-mediated urate transport and interacts with key residues within the URAT1 binding pocket. HYJ-2 reduces serum urate levels in hyperuricemic mice without inducing liver or kidney injury. HYJ-2 shows low cytotoxicity to hepatocytes and renal cells. HYJ-2 does not significantly induce hepatocyte apoptosis or mitochondrial dysfunction. HYJ-2 can be used in studies related to hyperuricemia and gout .
Cat. No.: HY-182046
CAS No.: 2930131-74-9
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HD202A is an orally active, selective dual inhibitor of MNK1/MNK2 (with IC50 values of 6.09 nM and 8.06 nM, and Kd values of 1.913 μM and 5.244 μM, respectively) that inhibits the MNK-eIF4E signaling pathway. By downregulating perilipin 2 and SCD1, while upregulating adipose triglyceride lipase and PPARγ coactivator 1α, HD202A enhances mitochondrial fatty acid oxidation and redox homeostasis. HD202A effectively suppresses body weight gain, hepatic lipid accumulation and elevation of serum lipids, significantly improves glucose tolerance and insulin sensitivity of the organism, and ameliorates inflammatory features. With these comprehensive pharmacological activities, HD202A exhibits great application potential in studies of metabolic dysfunction-associated steatotic liver disease .
Cat. No.: HY-183456
CAS No.: 71308-35-5
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Tyrphostin AG17 is an orally active CDK2 inhibitor and EGFR tyrosine kinase antagonist. Tyrphostin AG17 reduces the levels of p21 and p16. Tyrphostin AG17 induces G1 phase cell cycle arrest, Apoptosis, mitochondrial dysfunction, decreased ATP levels, and inhibits DNA, RNA and protein synthesis, adipogenesis, and lipid synthesis. Tyrphostin AG17 inhibits fat accumulation, white adipose tissue hypertrophy, and alterations of glycogen and lipid inclusions in hepatocytes in obese mice without changing their serum biochemical parameters. Tyrphostin AG17 exhibits anticancer effects. Tyrphostin AG17 can be used in research related to immunoblastic lymphoma, leukemia, ovarian cancer, glioblastoma, colon cancer, breast cancer, melanoma, obesity and hepatic steatosis .
Cat. No.: HY-183309
Research Areas:
FXR/HSD17B13-modulator-2 is a dual FXR activator and HSD17B13 inhibitor with human FXR EC50 of 128 nM, human HSD17B13 IC50 of 0.18 μM, high selectivity over related nuclear receptors and HSD17B isoforms, and oral effectiveness.FXR/HSD17B13-modulator-2 alleviates fatty liver, regulates lipid metabolism, reduces inflammation, and attenuates hepatic fibrosis.FXR/HSD17B13-modulator-2 is the first non-carboxylic acid dual FXR/HSD17B13 modulator.FXR/HSD17B13-modulator-2 can be used for the research of metabolic dysfunction-associated steatohepatitis .
Cat. No.: HY-184158
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HATC is a HIF-1α AUTAC degrader. HATC links HIF-1α to LC3 to form a ternary complex that undergoes degradation via the autophagy-lysosome fusion pathway. HATC induces dose-dependent HIF-1α degradation in multiple cell types. HATC reduces visceral fat accumulation, hepatic lipid deposition, senescent cell aggregation, and bone loss; alleviates age-related intervertebral disc degeneration, liver dysfunction, kyphosis, and alveolar dilation; decreases circulating lactic acid levels; improves physical performance; and reverses age-related changes in granulocyte proportions. HATC extends median and maximum lifespan, reduces transcriptomic age, and causes no obvious persistent toxicity. HATC can be used in the research of age-related diseases (pink: LC3 ligand (HY-50759); blue: HIF-1α ligand (HY-P10426); Linker: (HY-W008264)) .
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Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
