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HSV-TK substrate Sale

目录号 : GC36260

HSV-TK substrate 是 HSV-TK 的底物,并在表达 HSV-T K 和 bystander 细胞中诱导 multi-log 细胞毒性,具有抗肿瘤活性。

HSV-TK substrate Chemical Structure

Cas No.:111687-37-7

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Sample solution is provided at 25 µL, 10mM.

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产品描述

HSV-TK substrate is a substrate for HSV-TK, and induces multi-log cytotoxicity in HSV-TK-expressing and bystander cells. HSV-TK substrate shows antitumor activity[1].

[1]. Shewach DS, et al. Multi-log cytotoxicity of carbocyclic 2'-deoxyguanosine in HSV-TK-expressing human tumor cells. Hum Gene Ther. 2002 Mar 1;13(4):543-51.

Chemical Properties

Cas No. 111687-37-7 SDF
Canonical SMILES O=C1NC(N)=NC2=C1N=CN2[C@H]3[C@H](O)[C@H](O)[C@@H](CO)C3
分子式 C11H15N5O4 分子量 281.27
溶解度 Soluble in DMSO 储存条件 Store at -20°C
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 3.5553 mL 17.7765 mL 35.553 mL
5 mM 0.7111 mL 3.5553 mL 7.1106 mL
10 mM 0.3555 mL 1.7777 mL 3.5553 mL
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Research Update

Unrepairable DNA double-strand breaks initiate cytotoxicity with HSV-TK/ganciclovir

Cancer Gene Ther 2011 Oct;18(10):751-9.PMID:21869826DOI:10.1038/cgt.2011.51.

The herpes simplex virus thymidine kinase (HSV-TK) is the most widely used suicide gene in cancer gene therapy due to its superior anticancer activity with ganciclovir (GCV) compared with other HSV-TK substrates, such as 1-β-D-arabinofuranosyl thymine (araT). We have evaluated the role of DNA damage as a mechanism for the superiority of GCV. Using γ-H2AX foci as an indicator of DNA damage, GCV induced ≥ sevenfold more foci than araT at similar cytotoxic concentrations. The number of foci decreased after removal of either drug, followed by an increase in Rad51 foci indicating that homologous recombination repair (HRR) was used to repair this damage. Notably, only GCV produced a late and persistent increase in γ-H2AX foci demonstrating the induction of unrepairable DNA damage. Both drugs induced the ATR damage response pathway, as evidenced by Chk1 activation. However, GCV resulted in greater activation of ATM, which coincided with the late induction of γ-H2AX foci, demonstrating the presence of DNA double-strand breaks (DSBs). The increase in DSBs after Rad51 induction suggested that they occurred as a result of a failed attempt at HRR. These data demonstrate that the late and unrepairable DSBs observed uniquely with GCV account for its superior cytotoxicity and further suggest that inhibition of HRR will enhance cytotoxicity with HSV-TK/GCV.