c 225

Cetuximab (C225) 属于单克隆抗体，是一种人源表皮生长因子受体 (EGFR) 的抑制剂 (Kd=0.201 nM)。Cetuximab 具有抗肿瘤活性，可以抑制肿瘤细胞增殖，诱导细胞凋亡。

ENT-C225 是一种高效的 TrkB 神经营养素受体（TrkBR）激活剂，具有神经保护活性，可用于研究阿尔茨海默病和帕金森病。

DAC-2-25是 Hydra 头部再生调节剂。它通过诱导 Hydra 的同源转化而起作用。

UNC2250 是选择性的Mer 抑制剂，其IC50=1.7 nM，分别比相关的激酶 Axl 和 Tyro3 选择性高 160 倍和 60 倍。

Docosapentaenoic acid (C22:5)，也叫做Clupanodonic acid和二十二碳五烯酸，是一种多不饱和脂肪酸。全顺式 4,7,10,13,16-DPA在神经保护、抗癌和抗炎等方面具有重要作用，包括调节血脂、软化血管、降低血液粘度、改善视力、促进生长发育和提高人体免疫功能。

Lansoprazole sulfide (AG-1777，兰索拉唑硫醚)是Lansoprazole的活性代谢物，具有相似的活性。Lansoprazole是一种质子泵抑制剂和抗结核剂，对 Mycobacterium tuberculosis 的 IC50= 0.59 µM。

N-Nitroso sarcosine is a carcinogen and nitrosation product of sarcosine that has been found in cured meat products.1,2In vivo, N-nitroso sarcosine (225 mg kg) induces the formation of metastatic liver carcinomas in mice.2 1.Janzowski, C., Eisenbrand, G., and Preussmann, R.Occurrence of N-nitrosamino acids in cured meat products and their efffect on formation of N-nitrosamines during heatingFood Cosmet. Toxicol.16(4)343-348(1978) 2.Wogan, G.N., Paglialunga, S., Archer, M.C., et al.Carcinogenicity of nitrosation products of ephedrine, sarcosine, folic acid, and creatinineCancer Res.35(8)1981-1984(1975)

Ara-G 是一种脱氧鸟苷 (GdR) 类似物和核苷类似物，可被 T 淋巴谱系细胞迅速转化为其相应的阿拉伯糖基鸟嘌呤核苷酸三磷酸 (araGTP)，从而抑制 DNA 合成和对 T 淋巴母细胞的选择性体外毒性细胞系以及来自 T 细胞急性淋巴细胞白血病 (ALL) 患者的新鲜分离的白血病细胞。

Purfalcamine is an orally active, selective Plasmodium falciparum calcium-dependent protein kinase 1 (PfCDPK1) inhibitor with an IC50 of 17 nM and an EC50 of 230 nM. Purfalcamine has antimalarial activity and causes malaria parasites developmental arrest at the schizont stage[1][2]. Purfalcamine has low activity against Toxoplasma gondii calcium-dependent protein kinase 3 (TgCDPK3)[1]. Purfalcamine (225, 450 nM) has no effect on the parasitemia in the first 32 hours. After about 40 hours, parasite level remains stable and then begins dropping[1]. Purfalcamine inhibits proliferation with EC50s of 171-259 nM for P. falciparum strains (3D7, Dd2, FCB, HB3 and W2), which indicates effectiveness against drug-resistant parasites[1]. Given that the EC50 value for P. falciparum (3D7) is 230 nM, Purfalcamine shows a therapeutic window ranging from 23-fold to 36-fold (EC50s for CHO=12.33 μM, HEp2=7.235 μM, HeLa=7.029 μM and Huh7=5.476 μM)[1]. Purfalcamine (10 mg kg; oral gavage; BID; for 6 days) demonstrates a delay in the onset of parasitemia in treated mice[1]. Purfalcamine (20 mg kg; orally gavage) exhibits a Cmax of 2.6 μM with a half-life of 3.1 hours[1]. Animal Model: Male BALB c mice, 7 weeks of age with the malaria parasite[1] [1]. Nobutaka Kato, et al. Gene expression signatures and small-molecule compounds link a protein kinase to Plasmodium falciparum motility. Nat Chem Biol. 2008 Jun;4(6):347-56. [2]. Rajshekhar Y Gaji, et al. Expression of the essential Kinase PfCDPK1 from Plasmodium falciparum in Toxoplasma gondii facilitates the discovery of novel antimalarial drugs. Antimicrob Agents Chemother. 2014 May;58(5):2598-607.