Hepatotoxicity

DI-1859 is a DCN1 and cullin 3 inhibitor with a K_i of <1 nM against human DCN1. DI-1859 forms a covalent bond with Cys115 of DCN1, cleaves its dimethylamino group, disrupts the DCN1-UBC12 interaction, and selectively inhibits the neddylation modification of cullin 3 relative to other cullins. DI-1859 inactivates CRL3, promotes the accumulation of NRF2 and SLC7A11, upregulates the expression of HO-1 and NQO1, reduces reactive oxygen species (ROS) levels, enhances insulin signaling, promotes insulin secretion, activates RhoA, regulates the phosphorylation of AKT, without completely blocking the neddylation modification of cullin 3 or restoring the expression of IRS-1. DI-1859 can be used in the research of Acetaminophen (HY-66005)-induced hepatotoxicity, hyperglycemia, metabolic dysfunction-associated steatotic liver disease, insulin resistance, breast cancer and lung cancer.

Spinacetin is an orally active flavonoid glycoside found in Inula japonica, with antioxidant and anti-inflammatory activities. Spinacetin inhibits major inflammatory signaling pathways such as Syk, MAPK, and NF-κB, and reduces Ca²⁺-dependent release of allergic mediators. Spinacetin induces protective autophagy and enhances antioxidant defense by upregulating SIRT3/SIRT1/PGC-1α, activating AMPK, and inhibiting mTOR and NF-κB, thereby exerting anti-apoptotic, cardioprotective, bladder-protective, and hepatoprotective effects. Spinacetin alleviates Doxorubicin (HY-15142A)-induced cardiotoxicity and reduces Cyclophosphamide (HY-17420)-induced hemorrhagic cystitis. Spinacetin can be used in research on allergic reactions, cardiotoxicity, cystitis, and cadmium-aggravated hepatic ischemia.

Octylamine (n-Octylamine) is a positive effector of FMO. Octylamine interacts with oxidized cytochrome P-450 to produce a type II difference spectrum that is blocked by carbon monoxide. Octylamine enhances N-deacetyl ketoconazole-induced LDH leakage in cell cultures, but does not interfere with the LDH assay. Octylamine can be used in hepatotoxicity research.

Dimethoxycurcumin (DiMC) is a curcuminoid compound found in Curcuma longa. Dimethoxycurcumin is also an orally active thioredoxin reductase inhibitor (IC₅₀ = 5.4 μM) and androgen receptor antagonist. Dimethoxycurcumin inhibits thioredoxin reductase, leading to oxidized thioredoxin accumulation, ROS production, DNA damage, glutathione depletion, mitochondrial membrane potential decrease, ATP depletion, S phase arrest, and apoptosis. Dimethoxycurcumin inhibits NF-κB, NADPH oxidase subunits, ATP synthase subunits, CDK4, cyclin-D1, FASN, ACC, and the IRS2-PI3K-Akt pathway, while activating AMPK, ERK, and JNK. Dimethoxycurcumin can be used for research on cancer, arsenic-induced hepatotoxicity, and tuberculosis.

Prothioconazole is an orally active broad-spectrum fungicide. Prothioconazole weakly inhibits CaCYP51 activity in Candida albicans, with an apparent IC₅₀ of approximately 120 μM. Prothioconazole disrupts Microtubule stability by reducing the acetylation level of α-tubulin. Prothioconazole induces Mitochondrial dysfunction, oxidative stress, DNA damage, and Apoptosis. Prothioconazole accumulates ¹⁴-methylated sterols and depletes ergosterol in cells, culture media, plants, and animals. Prothioconazole interferes with pyruvate metabolism and glycolysis/gluconeogenesis processes in mouse liver, downregulates Fasn mRNA expression, and induces hepatotoxicity and renal metabolic disorders. Prothioconazole reduces the fertility of female mice. Prothioconazole inhibits body weight gain and increases liver/kidney indices in mice. Prothioconazole can be used in studies related to candidiasis.

Nodularin is a hepatotoxin, tumor promoter, and protein phosphatase inhibitor. Nodularin induces apoptosis (apoptosis) in normal cells (including caspase activation, upregulation of Bcl-XS, and upregulation of BAX/P53), triggers hyperphosphorylation of the MAPK/ERK, mTOR/S6K and p38 MAPK signaling pathways, and induces oxidative stress, endoplasmic reticulum membrane instability, peroxisome proliferation and increased lysosomal enzyme activity. Nodularin promotes DEN (HY-N7434)-initiated hepatocyte proliferation and adenoma formation, and inhibits proliferation, phagocytosis and chemotaxis of normal lymphocytes, oocyte maturation and vitellogenesis, as well as angiogenesis. Nodularin exhibits hepatotoxicity, reproductive and endocrine toxicity, and embryonic developmental toxicity in various animal models. Nodularin can be used in studies related to liver cancer, hepatotoxicity and reproductive endocrine toxicity.

Dimethoxycurcumin-d₆ (DiMC-d₆; CHC 004-d₆; Di-O-methylcurcumin-d₆) is the deuterated-labeled Dimethoxycurcumin (HY-100977). Dimethoxycurcumin (DiMC) is a curcuminoid compound found in Curcuma longa. Dimethoxycurcumin is also an orally active thioredoxin reductase inhibitor (IC₅₀ = 5.4 μM) and androgen receptor antagonist. Dimethoxycurcumin inhibits thioredoxin reductase, leading to oxidized thioredoxin accumulation, ROS production, DNA damage, glutathione depletion, mitochondrial membrane potential decrease, ATP depletion, S phase arrest, and apoptosis. Dimethoxycurcumin inhibits NF-κB, NADPH oxidase subunits, ATP synthase subunits, CDK4, cyclin-D1, FASN, ACC, and the IRS2-PI3K-Akt pathway, while activating AMPK, ERK, and JNK. Dimethoxycurcumin can be used for research on cancer, arsenic-induced hepatotoxicity, and tuberculosis.

Chlorfluazuron (IKI-7899) is a benzoylurea chitin synthesis inhibitor and a PPARγ agonist ligand that blocks the polymerization of UDP-N-acetylglucosamine by inhibiting chitin synthase, disrupting cuticle formation, molting, and embryonic development, thereby exerting ovicidal, larvicidal, and fecundity-reducing effects in insects. Chlorfluazuron is used in hepatotoxicity research.

D-Tetramethrin is a type I synthetic pyrethroid insecticide and hepatotoxicity inducer. D-Tetramethrin induces oxidative stress in the liver of zebrafish. D-Tetramethrin induces Apoptosis and inflammatory responses. D-Tetramethrin causes severe liver damage in zebrafish. D-Tetramethrin can be used in studies related to hepatotoxicity.

Chlorfluazuron (Standard) (IKI-7899 (Standard)) is the analytical standard of Chlorfluazuron (HY-133204). This product is intended for research and analytical applications. Chlorfluazuron (IKI-7899) is a benzoylurea chitin synthesis inhibitor and a PPARγ agonist ligand that blocks the polymerization of UDP-N-acetylglucosamine by inhibiting chitin synthase, disrupting cuticle formation, molting, and embryonic development, thereby exerting ovicidal, larvicidal, and fecundity-reducing effects in insects. Chlorfluazuron is used in hepatotoxicity research.

Fluindarol is a phenylindandione derivative and an orally active anticoagulant. Fluindarol acts as a toxicant that induces organ and tissue haemorrhages and liver parenchymal necrosis in rats. Fluindarol exhibits acute and cumulative preclinical toxicity in rats, rabbits, and dogs, with higher toxicity in female rats than male rats. Fluindarol lacks analgesic action, produces only minor blood pressure effects, and does not alter circulation, respiration, CNS, or cardiac activity. Fluindarol is considered too toxic for clinical use based on preclinical data.

Chitohexaose hexahydrochloride is a small molecular polysaccharide. Chitohexaose hexahydrochloride inhibits the binding of AgW to TLR4. Chitohexaose hexahydrochloride upregulates IL-10, inhibits LPS-induced upregulation of ROS, induces alternative activation of macrophages/monocytes, and suppresses LPS-induced production of TNF-α, IL-1β and IL-6. Chitohexaose hexahydrochloride reverses the mortality of mice challenged with APAP or LPS. Chitohexaose hexahydrochloride can be used in research related to Acetaminophen (HY-66005)-induced hepatotoxicity and endotoxemia.