inflamed

BAY-1797 是具有口服活性的选择性P2X4高效拮抗剂，对人 P2X4 的IC50为 211 nM，具有抗伤害和抗炎作用。

5-Acetylsalicylic acid (5-acetyl-2-hydroxybenzoic acid) 是炎症性肠病中的活性剂，具有抗炎活性。

ASIC blocker (IC50 values are 0.44, 2.1 μM and no effect at rat ASIC1a, ASIC3 and ASIC2a, respectively: IC50 value = 0.12 μM at human ASIC1a with no effect at ASIC2a or ASIC3). Inhibition was also observed at heteromeric ASIC channels (IC50 values are 0.79, 0.87 and 4.5 uM at rat ASIC1a+3, ASIC1a+2a and ASIC2a+3; IC5O values are 0.33 and 0.69 uM at human ASIC1a+2a and ASIC1a+3, with no effect at ASIC2a+3). Attenuates pathophysiological nociceptive behaviors in CFA-inflamed and CCI rats.

TOP1288是一种窄谱激酶抑制剂，抑制P38α、Src和Syk激酶活性，IC50分别为116 nM、24 nM和659 nM。TOP1288还能抑制发炎活检组织和肌成纤维细胞释放炎症细胞因子。

Phenylbutazone-d9 is intended for use as an internal standard for the quantification of phenylbutazone by GC- or LC-MS. Phenylbutazone is a non-steroidal anti-inflammatory drug and an inhibitor of the peroxidase activity of COX (IC50 = ~100 µM in the presence of hydrogen peroxide). It also inhibits prostaglandin I synthase (IC50 = ~25 µM in the presence of hydrogen peroxide). Phenylbutazone (2 mg kg) reduces increases in type II collagen levels in the inflamed joints of an equine model of LPS-induced acute synovitis. Formulations containing phenylbutazone have been used in the treatment of lameness in horses.

GSK2239633 is a potent CC-chemokine receptor 4 antagonist with pIC50 of 7.9. The CC-chemokine receptor 4 (CCR4) is thought potentially to play a critical role in asthma pathogenesis due to its ability to recruit type 2 T-helper lymphocytes to the inflamed airways. Therefore, CCR4 provides an excellent target for anti-inflammatory therapy.

Resolvins are a family of potent lipid mediators derived from both eicosapentaenoic acid and docosahexaenoic acid.[1] In addition to being anti-inflammatory, resolvins promote the resolution of the inflammatory response back to a non-inflamed state.[2] Resolvin D1 is produced physiologically from the sequential oxygenation of DHA by 15- and 5-lipoxygenase.[1] 17(R)-RvD1 is an aspirin-triggered epimer of RvD1 that reduces human polymorphonuclear leukocyte (PMN) transendothelial migration, the earliest event in acute inflammation, with equipotency to RvD1 (EC50 = ~30 nM).[3] 17(R)-RvD1 exhibits a dose-dependent reduction in leukocyte infiltration in a mouse model of peritonitis with maximal inhibition of ~35% at a 100 ng dose.[3] In contrast to RvD1, the aspirin-triggered form resists rapid inactivation by eicosanoid oxidoreductases. Analytical and biological comparisons of synthetic 17(R)-RvD1 with endogenously derived 17(R)-RvD1 have confirmed its identity as matching the natural product.[4]

Zn-DPA-maytansinoid conjugate 1 为一种靶向小分子免疫检查点的类美坦素偶联物。其能持续诱导肿瘤生长消退，并激活肿瘤微环境（TME），转化为“炎热肿瘤”。

Resolvins are a family of potent lipid mediators derived from both eicosapentaenoic acid and docosahexaenoic acid . [1] In addition to being anti-inflammatory, resolvins promote the resolution of the inflammatory response back to a non-inflamed state.[2] Resolvin D5 (RvD5) is a DHA-derived resolvin generated by a double dioxygenation mechanism.[3] RvD5 has been identified in media from ionophore-stimulated trout brain cells, in human synovial fluid from patients with rheumatoid arthritis, and in exudates of bacterial infections in mice. [4][5][6] RvD5 stimulates the phagocytosis of E. coli by human macrophages, and RvD5 methyl ester enhances bacterial killing in mice inoculated with E. coli. [6] Analytical and biological comparisons of synthetic RvD5 with endogenously derived RvD5 have confirmed its identity as matching the natural product.[7]

ACT-672125 is a Potent CXCR3 Antagonist with Therapeutic Potential in Autoimmune Diseases. ACT-672125 showed good physicochemical properties and safety profile. In a proof-of-mechanism model of lung inflammation, ACT-672125 inhibited the recruitment of CXCR3 expressing T cells into the inflamed lung in a dose-dependent manner.