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Evofosfamide

CAS No. : 918633-87-1

MCE 国际站：Evofosfamide

产品活性：Evofosfamide (TH-302) 是一种缺氧 (hypoxia) 激活前体，缺氧 (N₂) 和常氧 (21% O₂) 环境下，IC₅₀ 分别为 10 μM 和 1000 μM。

研究领域：Apoptosis

作用靶点：Apoptosis

In Vitro: Evofosfamide (TH-302) induces γH2AX and apoptosis. Evofosfamide displays hypoxia-selective and concentration-dependent cytotoxic activity that is comparable in both p53-proficient and -deficient cells. Treatment with Evofosfamide (TH-302) alone causes an accumulation of G₂/M cells. Inhibition of Chk1 by PF47736 in cells treated with Evofosfamide reduces Evofosfamide (TH-302)-mediated G₂/M arrest under both normoxia and hypoxia.

In Vivo: Evofosfamide (TH-302) is a hypoxia-activated prodrug known to activate selectively under the hypoxic conditions commonly found in solid tumors. The mean values of normalized K^trans decrease 69.2% for Evofosfamide (TH-302)-treated mice in Hs766t tumors, decrease 46.1% for Mia PaCa-2 tumors and increase 4.9% in SU.86.86 tumors. Both changes for Hs766t and Mia PaCa-2 treatment groups are statistically significant (P<0.01) when compare to their own control group. A significant reduction in the hypoxic fraction (HF) to 2.1%±4.7% is seen after 95% oxygen breathing (P<0.001), whereas 7% oxygen breathing significantly increase the HF to 29.5%±14.7% (P=0.029). Exposing rhabdomyosarcoma-bearing rats to increasing oxygen conditions abolish the effect of TH-302 and reduce the T4×SV from 20.4±3.5 to 15.3±2.5 days (P=0.007), whereas control animals have an increased T4×SV. Upon combination with radiotherapy, the T4×SV of TH-302-treated tumors decrease from 30.8±5.9 (Evofosfamide (TH-302)+radiotherapy) to 25.7±2.9 days (Evofosfamide (TH-302)+radiotherapy+95% O₂).

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