342 Results for "

K Channel

" in MedChemExpress (MCE) Product Catalog:
Products (342)

342 Results for "K Channel" in MCE Product Catalog:

製品番号: HY-15026
CAS 番号: 915798-75-3
Target:  

Endogenous Metabolite

研究分野:  

Inflammation/Immunology

ATB-429, a novel H2S-releasing derivative of mesalamine, demonstrates significant anti-nociceptive and anti-inflammatory effects in models of irritable bowel syndrome (IBS). By releasing hydrogen sulfide (H2S), ATB-429 modulates colorectal distension-induced hypersensitivity in both healthy and postcolitic rats. It attenuates abdominal withdrawal responses and suppresses spinal c-Fos mRNA expression, indicating its potential to alleviate pain associated with gastrointestinal inflammation. Moreover, ATB-429 down-regulates colonic cyclooxygenase-2 and interleukin-1β mRNA expression, effects not observed with mesalamine alone. The mechanism involves ATP-sensitive K+ (KATP) channels, as evidenced by reversal of ATB-429's effects with glibenclamide. These findings suggest ATB-429 could offer therapeutic benefits for managing painful intestinal disorders linked to inflammation .
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製品番号: HY-W027553S1
別名: NIK-247-d9 free base
Ipidacrine-d9 (NIK-247-d9 (free base)) is the deuterium labeled Ipidacrine (HY-W027553). Ipidacrine is orally active and brain-penetrant AChE and BuChE inhibitors with IC50 values of 1 μM and 1.9 μM, respectively, which is also a partial agonist of M2-cholinergic receptors and a reversible cholinesterase inhibitor. Ipidacrine has a stimulating effect on neuromuscular transmission and excitation along the nerve fibres with a moderately anti-pain effect. Ipidacrine is an aminopyridines and is structurally similar to Tacrine (HY-111338). Ipidacrine is effective in various amnesia models, improves erectile function and inhibits K+ and Na+-channels in the neuronal membrane in diabetic rats. Ipidacrine is promising for research of Alzheimer’s disease, ischaemic stroke, idiopathic neuropathy of the facial nerve, diabetes mellitus-induced erectile dysfunction and other deficits in central or peripheral cholinergic deseases .
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