Tezacitabine is a cytostatic and cytotoxic antimetabolite and a nucleoside analogue with a dual mechanism of action that irreversibly inhibits ribonucleotide reductase and can be incorporated into DNA during replication or repair, causing DNA chain termination. It blocks tumor cells in the G1 and S phases of the cell cycle, inducing apoptotic cell death, with potential applications in treating leukemia and solid tumors[1][2].

Tezacitabine (0.01-10 μM; 24 hours; CCRF-SB, KG-1, Jurkat, COLO-205, MCF-7 and PC-3 cells) treatment leads to the G1 and S-phase leaky block of the cell cycle [1]. Tezacitabine (0.01-10 μM; 24 hours; CCRF-SB, KG-1, Jurkat, COLO-205, MCF-7 and PC-3 cells) treatment concentration-dependently apoptosis the cells by the caspase 3/7 pathway[1]. Tezacitabine has highly cytostatic and cytotoxic properties. The cytotoxic effect of tezacitabine is manifested not only in apoptosis but also in changes in protein metabolism[1]. Cell Cycle Analysis [1] Cell Line: CCRF-SB, KG-1, Jurkat, COLO-205, MCF-7 and PC-3 cells Concentration: 0.01 μM, 0.1 μM, 1.0 μM, and 10 μM Incubation Time: 24 hours Result: Induced leaky block of the G1 (at concentrations higher than 10 nM) and S-phase (at low concentration) of the cell cycle. Apoptosis Analysis [1] Cell Line: CCRF-SB, KG-1, Jurkat, COLO-205, MCF-7 and PC-3 cells Concentration: 0.01 μM, 0.1 μM, 1.0 μM, and 10 μM Incubation Time: 24 hours Result: Concentration-dependently induced apoptotic death of cells by the caspase 3/7 pathway.

Tezacitabine (100 mg/kg; intraperitoneal injection; daily; female nude mice) treatment inhibits tumor growth in HCT 116 tumor xenografts over 14 days in 7-9-week-old female nude mice injected with HCT 116 cells [2].