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Targaprimir-96

CAS No. : 1655508-14-7

MCE 站：Targaprimir-96

产品活性：Targaprimir-96 是 microRNA-96 (miR-96) 加工的有效抑制剂。Targaprimir-96 选择性地调节癌细胞中 miR-96 的产生并触发凋亡 (apoptosis)。Targaprimir-96 高亲和力的与 primary miR-96 (pri-miR-96) 结合。Targaprimir-96 直接与乳腺癌细胞中的 pri-miR-96 结合，并不影响健康乳腺细胞。

研究领域：Epigenetics  |  Apoptosis

作用靶点：MicroRNA  |  Apoptosis

In Vitro: Targaprimir-96 shows a dose-response in MDA-MB-231 triple negative breast cancer cells with an IC₅₀ of ~50 nM by assessing the reduction of mature miR-96 levels. Targaprimir-96 (50 nM) boosts the amount of the pri-miRNA and decreases the levels of the pre-miRNA and mature miRNA in a dose-dependent manner.
Targaprimir-96 (50 nM; 48 hours) increases FOXO1 levels and triggers apoptosis in breast cancer cell line 4175.
Targaprimir-96 binds RNA3 (contains both the Drosha site and the adjacent 1×1 nt GG internal loop) with a K_d of 85 nM. Targaprimir-96 binds RNA1, RNA2, RNA4, and RNA5 with K_d values of 1.2, 0.9, 1.2, and 1.5 μM, respectively. Thus, Targaprimir-96 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.

In Vivo: Targaprimir-96 (10 mg/kg; i.p.; every other day for 21 days) inhibits tumor growth in a mouse model of triple-negative breast cancer (TNBC).
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 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.

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