as 183

AS 183 is an inhibitor of cholesterol acyltransferase (ACAT).

SSJ-183 是一种低毒性和可口服的和抗疟疾药物，对恶性疟原虫的IC50=7.6 nM，高达2000 mg kg po的剂量没有致死性。

Poloxamer 183 L63 是一种由聚氧乙烯和聚氧丙烯组成的嵌段聚合物，平均分子量为2000。在浓度为1 mg mL时，该化合物对Mycobacterium avium表现出83%的抑菌活性。Poloxamer 183 L63 能形成热可逆水凝胶，被用于食品添加剂，并在化妆品、药品和组织工程中作为药物输送载体。

SBI-183 是一种具有口服活性的 QSOX1 抑制剂 (Kd: 20 μM)，能够抑制肾癌细胞系、三阴性乳腺癌细胞系、肺腺癌细胞系和胰腺导管腺癌的增殖与侵袭表型。SBI-183 在体内可以抑制两种人肾细胞癌异种移植小鼠模型的肿瘤生长。

CRBN ligand-183 是一种CRBN型E3泛素连接酶配体，用于制备PROTAC。

(Z)-Tyrphostin A51 是 Lanoconazole A51 的 Z 构型形式。Tyrphostin A51 是一种有效的蛋白酪氨酸激酶 (PTK)抑制剂，以剂量依赖性方式抑制原代星形胶质细胞培养物中 [3H]牛磺酸的体积敏感释放。Tyrphostin A51 显着降低细胞酪氨酰磷酸化水平。Tyrphostin A51 抑制基础和 EGF 诱导的人骨细胞增殖。

Anticancer agent 183 (compound 4h) exhibits potent inhibition of matrix metalloproteinase-9 (MMP-9), reducing its viability by more than 75% at a concentration of 100 μg mL. Additionally, it demonstrates significant anticancer activity, with an IC50 value of <0.14 μM against the A549 cell line and induces apoptotic [1] processes.

GPR183 antagonist-2 (化合物 32) 是一种选择性GPR183拮抗剂，水溶性好，药代动力学特性优异。该化合物能剂量依赖性地减轻胶原诱导的关节炎(CIA)小鼠模型中的爪子和关节肿胀，并显著抑制促炎细胞因子(MCP-1，MMPs 和 VEGF)的基因表达。GPR183 antagonist-2 适用于自身免疫性疾病的研究。

GPR183-IN-2 (compound 23) 作为一种有效口服活性GPR183抑制剂，能够抑制Ca2+动员，其IC50为39.45 nM。该化合物在癌症、自身免疫疾病、疼痛及骨质疏松症研究中显示出潜在应用价值。

GPR183-IN-1 (compound 15) 是一种口服有效的GPR183抑制剂，具有抑制Ca2+动员的功能，IC50为39.97 nM。此化合物显示在癌症、自身免疫性疾病、疼痛以及骨质疏松症研究中具有应用潜力。

Anti-Mouse CXCR3 CD183 Antibody (CXCR3-173) 是一款源自美国仓鼠的IgG抗体抑制剂，专门针对小鼠CXCR3 CD183。

TCS 183 可以模拟 GSK3β 上的 Akt 磷酸化位点，阻止 LTD 的调节。

Leishmania peptide 183 is an antigen.

PI3Kα-IN-4 is a potent, selective and orally active inhibitor of PI3Kα, with an IC50 of 1.8 nM. PI3Kα-IN-4 has antitumor activity[1]. PI3Kα-IN-4 (compound 10) inhibits PI3Kα, β, δ, and γ, with IC50s of 1.8, 271.0, 13.9, and 13.8 nM, respectively in kinase assays[1].PI3Kα-IN-4 inhibits PI3Kα, β, δ, and γ, with IC50s of 12.1,1393, 183, and >10000 nM, respectively in cell based assays[1]. PI3Kα-IN-4 (compound 10) (30 mg kg; p.o. once daily for 21 d) achieves the best efficacy, which could inhibit tumor growth by 73.0% in mice[1].PI3Kα-IN-4 (15-40 mg kg; p.o. once daily for 30 d) dose dependently suppresses tumor growth by 62.5% (15 mg kg), 86.0% (30 mg kg) and 90.7% (40 mg kg), respectively in mice[1].PI3Kα-IN-4 (15-40 mg kg; p.o. once daily; 1-4 h) inhibits the phosphorylation of Akt in a dose- and time-dependent manner in vivo[1].PI3Kα-IN-4 shows high Cmax (mouse 22167, rat 2327 nM) and good bioavailability (mouse 59.4%, rat 46.9%) following oral administration (mouse 10, rat 3 mg kg)[1].PI3Kα-IN-4 shows t1 2 (mouse 0.99, rat 1.22 h) and low plasma clearance (mouse 4.16, rat 5.28 mL min kg) following intravenous injection (mouse 1, rat 1 mg kg)[1]. [1]. Dong J, et, al. Discovery of 3-Quinazolin-4(3 H)-on-3-yl-2, N-dimethylpropanamides as Orally Active and Selective PI3Kα Inhibitors. ACS Med Chem Lett. 2020 Jun 10; 11(7): 1463-1469.

PMX-205 is a cyclic hexapeptide that acts as a potent antagonist of C5a receptor (C5aR; IC50= 31 nM).1It is orally active and blocks inflammatory signaling and symptoms in animal models of colitis and allergic asthma.2,3PMX-205 is also brain penetrant and reduces neuroinflammation and neurodegeneration in an animal model of Alzheimer's disease.4 1.March, D.R., Proctor, L.M., Stoermer, M.J., et al.Potent cyclic antagonists of the complement C5a receptor on human polymorphonuclear leukocytes. Relationships between structures and activityMol. Pharmacol.65(4)868-879(2004) 2.Jain, U., Woodruff, T.M., and Stadnyk, A.W.The C5a receptor antagonist PMX205 ameliorates experimentally induced colitis associated with increased IL-4 and IL-10Br. J. Pharmacol.168(2)488-501(2013) 3.Staab, E.B., Sanderson, S.D., Wells, S.M., et al.Treatment with the C5a receptor/CD88 antagonist PMX205 reduces inflammation in a murine model of allergic asthmaInt. Immunopharmacol.21(2)293-300(2014) 4.Fonseca, M.I., Ager, R.R., Chu, S.-H., et al.Treatment with a C5aR antagonist decreases pathology and enhances behavioral performance in murine models of Alzheimer's diseaseJ. Immunol.183(2)1375-1383(2009)

NG 25 is a type II kinase inhibitor that inhibits MAP4K2 and TAK1 (IC50s = 21.7 and 149 nM, respectively).1It also inhibits the Src family kinases Src and LYN (IC50s = 113 and 12.9 nM, respectively) and Abl family kinases (IC50s = 75.2 nM), as well as CSK, FER, and p38α (IC50s = 56.4, 82.3, and 102 nM, respectively). NG 25 (100 nM) prevents TNF-α-induced IKKα/β phosphorylation and IκB-α degradation in L929 cells. It inhibits secretion of IFN-α and IFN-β induced by CpG type B and CL097, respectively, in Gen2.2 cells in a concentration-dependent manner.2NG 25 decreases cell viability of HCT116KRASWT, and to a greater degree of HCT116KRASG13D, colorectal cancer cells in a concentration-dependent manner.3It also reduces tumor growth and increases the number of TUNEL-positive tumor cells in a CT26KRASG12Dmouse orthotopic model of colorectal cancer. 1.Tan, L., Nomanbhoy, T., Gurbani, D., et al.Discovery of type II inhibitors of TGFβ-activated kinase 1 (TAK1) and mitogen-activated protein kinase kinase kinase kinase 2 (MAP4K2)J. Med. Chem.58(1)183-196(2015) 2.Pauls, E., Shpiro, N., Peggie, M., et al.Essential role for IKKβ in production of type 1 interferons by plasmacytoid dendritic cellsJ. Biol. Chem. 287(23)19216-19228(2012) 3.Ma, Q., Gu, L., Liao, S., et al.NG25, a novel inhibitor of TAK1, suppresses KRAS-mutant colorectal cancer growth in vitro and in vivoApoptosis24(1-2)83-94(2019)

Novel oxylipins, referred to as docosanoids, have been derived from C22polyunsaturated fatty acids 7(S),17(S)-dihydroxy-8(E),10(Z),13(Z),15(E),19(Z)-Docosapentaenoic acid (7(S),17(S)-hydroxy DPA) is a DPA-derived analog of the 17(S)-dihydroxy series of docosanoids known as protectins. Protectin D1, a DHA-derived dihydroxy fatty acid, exhibits potent anti-inflammatory activities.1,2,3Potentially, 7(S),17(S)-hydroxy DPA demonstrates similar properties; however, its biological activity has yet to be determined. 1.Serhan, C.N., Gotlinger, K., Hong, S., et al.Anti-inflammatory actions of neuroprotectin D1 protectin D1 and its natural stereoisomers: Assignments of dihydroxy-containing docosatrienesJ. Immunol.176(3)1848-1859(2006) 2.Ariel, A., and Serhan, C.N.Resolvins and protectins in the termination program of acute inflammationTRENDS in Immunology28(4)176-183(2007) 3.Schwab, J.M., Chiang, N., Arita, M., et al.Resolvin E1 and protectin D1 activate inflammation-resolution programmesNature447(7146)869-874(2007)

Rec 15/2615 is an antagonist of α1B-adrenergic receptors (α1B-ARs; Ki = 0.45 nM for the recombinant human receptor).1 It selectively inhibits α1B-ARs over α1A-, α1D-, and α1L-ARs (Kis = 7.59, 10.23, and 49 nM, respectively). Rec 15/2615 inhibits norepinephrine-induced contractions of isolated rabbit prostate and urethral strips (Kis = 100 and 316.2 nM, respectively), as well as reduces norepinephrine-induced contractions of chloroethylclonidine-precontracted isolated rabbit aortic rings (Ki = 50 nM).2 It decreases diastolic blood pressure (ED25 = 183 μg/kg, i.v.) and increases intracavernous pressure in anesthetized dogs when administered intracavernously at doses ranging from 30 and 1,000 μg/kg.1,2 |1. Sironi, G., Colombo, D., Poggesi, E., et al. Effects of intracavernous administration of selective antagonists of α1-adrenoceptor subtypes on erection in anesthetized rats and dogs. J. Pharmacol. Exp. Ther. 292(3), 974-981 (2000).|2. Testa, R., Guarneri, L., Angelico, P., et al. Pharmacological characterization of the uroselective alpha-1 antagonist Rec 15/2739 (SB 216469): Role of the alpha-1L adrenoceptor in tissue selectivity, part II. J. Pharmacol. Exp. Ther. 281(3), 1284-1293 (1997).