Targaprimir-96 TFA is a potent inhibitor ofmicroRNA-96 (miR-96) processing. Targaprimir-96 TFA selectively modulates miR-96 production incancercells and triggersapoptosis. Targaprimir-96 TFA binds primary miR-96 (pri-miR-96) with low nanomolar affinity. Targaprimir-96 TFA directly engages pri-miR-96 in breastcancercells and is ineffective on healthy breast cells^[1].

Targaprimir-96 TFA shows a dose-response in MDA-MB-231 triple negative breast cancer cells with an IC₅₀of ~50 nM by assessing the reduction of mature miR-96 levels. Targaprimir-96 (50 nM) TFA boosts the amount of the pri-miRNA and decreases the levels of the pre-miRNA and mature miRNA in a dose-dependent manner^[1].
Targaprimir-96 TFA (50 nM; 48 hours) increases FOXO1 levels and triggers apoptosis in breast cancer cell line 4175^[1].
Targaprimir-96 TFA binds RNA3 (contains both the Drosha site and the adjacent 1×1 nt GG internal loop) with a K_dof 85 nM. Targaprimir-96 binds RNA1, RNA2, RNA4, and RNA5 with K_dvalues of 1.2, 0.9, 1.2, and 1.5 μM, respectively. Thus, Targaprimir-96 TFA is highly RNA-selective and recognizes both the 1×1 nt GG and 1×1 nt UU loops to provide high affinity, effectively discriminating against a variety of related targets^[1].

Targaprimir-96 TFA (10 mg/kg; i.p.; every other day for 21 days) inhibits tumor growth in a mouse model of triple-negative breast cancer (TNBC)^[1].
The amount of Targaprimir-96 (2 or 7 mg/kg; i.p.) in plasma peaks is ~4 h in FVB/n mice. Importantly, even 48 hours postinjection, the concentration of Targaprimir-96 TFA remaining in plasma is much greater than the 50 nM cellular concentration that triggered apoptosis: 1.6 μM for the 2 mg/kg dosage and 1.9 μM for the 7 mg/kg dosage^[1].

1505.77

C₇₉H₁₀₃F₃N₁₈O₉

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