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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
268 Results for "
mitochondrial dysfunction
" in MedChemExpress (MCE) Product Catalog:
Products (268)
268 Results for "mitochondrial dysfunction" in MCE Product Catalog:
Cat. No.: HY-181477
Research Areas:
ERK5-IN-7 is an orally active ERK5 inhibitor with an IC50 of 403.4 nM. ERK5-IN-7 directly inhibits ERK5 kinase activity, and downregulates the phosphorylation level and total protein expression of ERK5. ERK5-IN-7 induces Apoptosis (upregulates Bax, downregulates Bcl-2, and induces Caspase-3 cleavage). ERK5-IN-7 induces ROS accumulation. ERK5-IN-7 exhibits anticancer effects against Lewis lung cancer .
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-162802
PI3K/AKT-IN-4 (compound 3) is a diterpenoid that can be isolated from the roots and rhizomes of Salvia castanea Dielsf. PI3K/AKT-IN-4 has antitumor activity, inhibiting cell viability and proliferation (IC50=4.72 μM) and promoting apoptosis by blocking the G0/G1 phase of the Hep3B cell cycle, inducing mitochondrial dysfunction and oxidative stress. In addition, PI3K/AKT-IN-4 inhibits hepatocellular carcinoma by inhibiting the PI3K-Akt signaling pathway and binding to PARP1 and CDK2 targets .
Cat. No.: HY-174374
CAS No.: 3076446-44-8
Target:
Research Areas:
Topobexin is a TOP2B-selective inhibitor with IC50 values of 0.19 μM and 4.8 μM for TOP2B and TOP2A (DNA decatenation assay). Topobexin binds to non-homologous residues in the obex pocket and targets the ATPase domain of TOP2B. Topobexin prevents anthracycline-induced DNA double-strand break formation, apoptotic signaling mediated by caspase 3/7, 8 and 9, cardiomyocyte morphological changes, mitochondrial depolarization/loss, left ventricular systolic dysfunction, extracellular matrix remodeling, fibrotic alterations, and increases in plasma cardiac troponin T and BNP. Topobexin does not impair the antiproliferative effects of anthracyclines in cancer cells, exhibits no intrinsic cytotoxicity in cardiomyocytes, and is well tolerated in rabbits. Topobexin can be used in studies related to anthracycline-induced cardiotoxicity .
Cat. No.: HY-182046
CAS No.: 2930131-74-9
Research Areas:
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
Research Areas:
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-W010201R
CAS No.: 106-22-9
Synonyms: (±)-Citronellol (Standard); (±)-β-Citronellol (Standard)
Cat. No.: HY-W087008
CAS No.: 6515-36-2
Cat. No.: HY-W040255
CAS No.: 89947-79-5
Synonyms: PGPC
Cat. No.: HY-182360
Target:
PERK Eukaryotic Initiation Factor (eIF) Bcl-2 Family Apoptosis Reactive Oxygen Species (ROS) STING DNA/RNA Synthesis PD-1/PD-L1
Research Areas:
Cytisine-Platinum(IV) Prodrug-1 is a Pt(IV) prodrug incorporating the natural compound Cytisine (HY-N0175) with antiproliferative activity against tumor cells. Cytisine-Platinum(IV) Prodrug-1 promotes calcium transfer across the IP3R1-GRP75-VDAC1 axis to drive mitochondrial calcium overload. Cytisine-Platinum(IV) Prodrug-1 initiates unfolded protein response via PERK, eIF2α, ATF4, and CHOP to modulate Bcl-2 and Bax, triggering apoptosis. Cytisine-Platinum(IV) Prodrug-1 induces mitochondrial dysfunction, ROS production, reduced ATP synthesis, DNA damage, and S-phase cell cycle arrest. Cytisine-Platinum(IV) Prodrug-1 activates the cGAS-STING pathway, reduces PD-L1 expression, drives immunogenic cell death. Cytisine-Platinum(IV) Prodrug-1 exhibits high physiological stability, efficient cellular accumulation, and enhanced platinum-DNA binding, and inhibits tumor growth in mouse models with reduced systemic toxicity. Cytisine-Platinum(IV) Prodrug-1 can be used for the research of lung cancer .
Category:
other families Ketones, Aldehydes, Acids Plants Disease Research Fields Inflammation/Immunology
Target:
Cat. No.: HY-155718
fac-[Re(CO)3(L6)(H2O)][NO3] (compound 6), the rhenium(I) tricarbonyl aqua complex, is an anticancer agent associated with mitochondrial dysfunction. fac-[Re(CO)3(L6)(H2O)][NO3] is cytotoxic to prostate cancer cells, IC50=50 nM (PC-3 cells). fac-[Re(CO)3(L6)(H2O)][NO3] mainly accumulates in the nucleus, down-regulates ATP production in PC3 cells, and promotes apoptosis. However, fac-[Re(CO)3(L6)(H2O)][NO3] did not induce necrosis, pyrodeath and autophagy .
Cat. No.: HY-164548
CAS No.: 958888-32-9
WK88-1 is an apoptosis inducer and Hsp90 client protein inhibitor with antiproliferative and immunomodulatory activities. WK88-1 inhibits signaling pathways such as PI3K/Akt and NF-κB, and induces mitochondrial dysfunction and cell cycle arrest. WK88-1 effectively suppresses cancer cell migration and invasion, and reverses various EGFR mutations and resistance to Gefitinib (HY-50895). WK88-1 also regulates the differentiation of monocytes and dendritic cells, blocks the expression of multiple chemokines, inhibits immune cell migration and M1 marker transcription, and restores impaired endocytic activity. WK88-1 has been used in studies of breast cancer, non-small cell lung cancer with various EGFR mutations or Met amplification, and atherosclerosis and other related diseases .
Cat. No.: HY-W010201S
CAS No.: 220687-53-6
Synonyms: (±)-Citronellol-d6; (±)-β-Citronellol-d6
Cat. No.: HY-W010201S1
Synonyms: (±)-Citronelloll-d3; (±)-β-Citronelloll-d3
Cat. No.: HY-L263
89 compounds
Energy metabolism is the most fundamental biochemical process in living organisms, encompassing glycolysis, the TCA cycle, oxidative phosphorylation, the pentose phosphate pathway, and fatty acid oxidation. These core pathways directly regulate cell survival, proliferation, differentiation, and apoptosis. Dysregulation of energy metabolism is closely linked to major diseases including cancer, diabetes, obesity, cardiovascular diseases, neurodegenerative disorders, and ischemia‑reperfusion injury. Targeting these metabolic pathways has become a frontier in drug discovery and mechanistic research.
The MCE Energy Metabolite Compound Library features 89 structurally defined small‑molecule compounds. It covers energy substrates, pathway intermediates, coenzymes and redox carriers, nucleotide derivatives, and microenvironmental modulators. This library is applicable to research areas including tumor metabolism, insulin resistance, mitochondrial dysfunction, oxidative stress, neuroprotection, and cardiometabolic diseases, providing a high‑quality tool for mechanistic studies, biomarker discovery, and high‑throughput drug screening.
Cat. No.: HY-N17612
CAS No.: 366477-44-3
Target:
Cat. No.: HY-184587
Research Areas:
Antibacterial agent 356 is an orally active antibacterial agent. Antibacterial agent 356 binds to the Mrr1 transcription factor, inhibits the expression of the MDR1 efflux pump gene, reduces the efflux of Rhodamine 123, and increases the accumulation of intracellular substrates in drug-resistant Candida albicans cells. Antibacterial agent 356 induces mitochondrial membrane potential reduction and ROS accumulation in Candida albicans, inhibits the yeast-hypha transition process, and suppresses its biofilm formation. Antibacterial agent 356 reverses efflux pump-mediated drug resistance in azole-resistant Candida albicans with overexpressed Mdr1. Antibacterial agent 356 improves the survival rate of Galleria mellonella larvae infected with azole-resistant Candida albicans*CA632, and reduces the renal fungal load and renal tissue damage in infected BALB/c mice. Antibacterial agent 356 can be used for the research of Candida albicans infection .
Cat. No.: HY-184749
Target:
Research Areas:
Topoisomerase I-IN-24 (compound 5l) is a topoisomerase I (topoisomerase I) inhibitor. Topoisomerase I-IN-24 inhibits topoisomerase I activity in a concentration-dependent manner, suppresses cancer cell migration, induces apoptosis (apoptosis), and arrests the cell cycle at the G1 phase. Topoisomerase I-IN-24 can be used in the research of lung cancer, hepatocellular carcinoma and cervical adenocarcinoma .
Cat. No.: HY-187518
CAS No.: 3134912-65-2
Target:
Research Areas:
NMT-IN-9 is an arylpyrrolidone-based NMT inhibitor with an IC50 of 93.20 nM and a KD of 5.57 × 10 -9 M against NMT. NMT-IN-9 exhibits broad-spectrum antifungal activity against Candida albicans, Candida glabrata, Candida tropicalis, Cryptococcus neoformans and Aspergillus fumigatus, with an MIC of 2-16 μg/mL, and retains activity against fluconazole-resistant Candida isolates, with an MIC of 8-16 μg/mL. NMT-IN-9 induces intracellular ROS accumulation, mitochondrial membrane depolarization, DNA damage, apoptosis and necrotic cell death in fungal cells, and disrupts fungal cell integrity. NMT-IN-9 can be used for studies on NMT-targeted antifungal mechanisms and fluconazole-resistant Candida infections .
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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
