L-Isoleucine
Catalog No: CFN91723
L-Isoleucine often impacts muscle repair function, cirrhosis, obesity, cardiovascular disease, glucose and lipid metabolism, blood glucose levels and other conditions. L-Isoleucine administration can regulate the inflammatory response to protect against pathogens in vivo and in vitro, making it for research in dextran sulfate sodium (DSS) (HY-116282) -induced colitis.
IC50 & Target: Human Endogenous Metabolite
Lithocholic acid
Catalog No: CFN89170
Lithocholic acid is a toxic secondary bile acid, causes intrahepatic cholestasis, has tumor-promoting activity, its toxic effect can be protected after it activates the vitamin D receptor, PXR and FXR.Lithocholic acid is a vitamin D receptor (VDR) ligand, it can activate the VDR to block inflammatory signals in colon cells.
Lithospermic acid
Catalog No: CFN98546
Lithospermic acid has anti-HIV, antioxidant ,anti-inflammatory, and hepatoprotective effects, is a competitive inhibitor of xanthine oxidas (XO), can directly scavenge superoxide and inhibit superoxide production in vitro, and presents hypouricemic actions in vivo. Lithospermic acid has inhibitory effects on proliferation and migration of rat vascular smooth muscle cells, it has a preventive effect on the development of diabetic retinopathy. Lithospermic acid can attenuate 1-methyl-4-phenylpyridine-induced neurotoxicity by blocking neuronal apoptotic and neuroinflammatory pathways. Lithospermic acid can attenuate mesenteric ischemia reperfusion injury in rat intestines by increasing tissue SOD and GPx activities and decreasing MDA and MPO levels, also improves morphological alterations which occurred after periods of reperfusion.
L-Nicotine
Catalog No: CFN99512
Nicotine is a potent inhibitor of cardiac A-type K+ channels, with blockade probably due to block of closed and open channels, this action may contribute to the ability of nicotine to affect cardiac electrophysiology and induce arrhythmias.Nicotine is able to activate mitogenic signalling pathways, which promote cell growth or survival as well as increase chemoresistance of cancer cells, nicotine activates its downstream signalling to interfere with the ubiquitination process and prevent Bcl-2 from being degraded in lung cancer cells, resulting in the increase of chemoresistance.