Animal experiment:

Mice: CML mice are treated daily with acriflavine (8 mg/kg) or PBS via intraperitoneal injection, for 10 days starting from day 7 after bone marrow transplantation[2].

Acriflavine is a fluorescent dye for labeling high molecular weight RNA. It is also a topical antiseptic.

Acriflavine is identified as a potent inhibitor of the MCT4 that can inhibit the binding between Basigin and MCT4. Acriflavine significantly inhibits growth and self-renewal potential of several glioblastoma neurosphere lines[1]. The HIF-1 inhibitor acriflavine decreases survival and growth of CML cells. It targets stem cell potential of CML cells[2].

Acriflavine treatment inhibits intratumoral expression of VEGF and tumor vascularization[1]. In a murine CML model, acriflavine decreases leukemia development and reduces LSC maintenance[2]. Acriflavine retards tumor growth in a murine model of breast cancer. The combination of sunitinib with acriflavine significantly decreases vascular endothelial growth factor and TGF-β expression and reduces tumor vasculature followed by increased intratumor necrosis and apoptosis[3].

[1]. Voss DM, et al. Disruption of the monocarboxylate transporter-4-basigin interaction inhibits the hypoxic response, proliferation, and tumor progression. Sci Rep. 2017 Jun 27;7(1):4292. [2]. Cheloni G, et al. Targeting chronic myeloid leukemia stem cells with the hypoxia-inducible factor inhibitor acriflavine. Blood. 2017 Jun 2. pii: blood-2016-10-745588. [3]. Yin T, et al. HIF-1 Dimerization Inhibitor Acriflavine Enhances Antitumor Activity of Sunitinib in Breast Cancer Model. Oncol Res. 2014;22(3):139-45.