Antimalarial; autophagy inhibitor; endosomal acidification fusion inhibitor. In clinical trials (alongside hydroxychloroquine) for SARS-CoV-2 infection; multiple potential mechanisms, including inhibiting viral endocytosis; attenuating the "cytokine storm"; binding Sigma 1 receptor (SARS-CoV-2 Nsp6 protein interacts with the Sigma receptor). Gordon et al. bioRxiv, Mar 23 2020, https://doi.org/10.1101/2020.03.22.002386; Hu et al. Nat. Nanotechnol., Mar 23 2020, https://doi.org/10.1038/s41565-020-0674-9; Wang et al. Cell Res 30:269–271, Feb 4 2020, https://doi.org/10.1038/s41422-020-0282-0.; Schrezenmeier & Dörner Nat. Rev. Rheumatol., 16:155-166, March 2020, https://doi.org/10.1038/s41584-020-0372-x; Guy et al. Science, 368 829-830 May 22 2020, https://doi.org/10.1126/science.abb9332.
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- Applications:Approved drug (U.S.); now approved by US FDA for COVID-19
Biochemicals & reagents
1) Frieboes et al. (2014), chloroquine-mediated cell death in metastatic pancreatic adenocarcinoma through inhibition of autophagy; JOP, 15 189 2) Jiang et al. (2010), Antitumor and antimetastatic activities of chloroquine diphosphate in a murine model of breast cancer; Biomed. Pharmacother., 64 609 3) Choi et al. (2014), Chloroquine eliminates cancer stem cells through deregulation of Jak2 and DNMT1; Stem Cells, 32 2309. 4) Mulcahy Levy et al. (2014), Autophagy inhibition improves chemosensitivity in BRAFV600E brain tumors; Cancer Discov., 4 773
Chloroquine is an antimalarial drug. It inhibits autophagy in a variety of cell lines (1), induces cell death in breast cancer cell lines and displays antitumor and antimetastatic activity in mouse models of breast cancer (2). It also eliminates cancer stem cells via deregulation of Jak2 and DNMT13 and displays synergy when combined with the Raf inhibitor, vemurafenib, in brain tumor (4). This compound is cell permeable and active in vivo.