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JPM-OEt is a broad spectrum cysteine cathepsin inhibitor. JPM-OEt binds covalently in the active site, and irreversibly inhibits the cysteine cathepsin family. Antitumor activity[1][2].

JPM-OEt (50 mg/kg; i.p.; daily for 30 days) reduces tumor cathepsin B activity significantly[1].JPM-OEt (50 mg/kg; i.p.; twice daily for 4 weeks) leads to tumor regression in the RIP1-Tag2 (RT2) mouse model of pancreatic islet cell tumorigenesis[2].JPM-OEt (50 mg/kg; i.p.; daily from 63 to 98 days) causes a significant delay in the increase of tumour burden during the first 2 weeks of treatment[3]. Animal Model: Female mice of a transgenic mouse[3]

[1]. Withana NP, et al. Cathepsin B inhibition limits bone metastasis in breast cancer. Cancer Res. 2012 Mar 1;72(5):1199-209. [2]. Bell-McGuinn KM, et al. Inhibition of cysteine cathepsin protease activity enhances chemotherapy regimens by decreasing tumor growth and invasiveness in a mouse model of multistage cancer. Cancer Res. 2007 Aug 1;67(15):7378-85. [3]. Schurigt U, et al. Trial of the cysteine cathepsin inhibitor JPM-OEt on early and advanced mammary cancer stages in the MMTV-PyMT-transgenic mouse model. Biol Chem. 2008 Aug;389(8):1067-74.