Ara-G 是一种脱氧鸟苷 (GdR) 类似物和核苷类似物，可被 T 淋巴谱系细胞迅速转化为其相应的阿拉伯糖基鸟嘌呤核苷酸三磷酸 (araGTP)，从而抑制 DNA 合成和对 T 淋巴母细胞的选择性体外毒性细胞系以及来自 T 细胞急性淋巴细胞白血病 (ALL) 患者的新鲜分离的白血病细胞。

Ara-G is a deoxyguanosine (GdR) analog and a nucleoside analogue that is rapidly converted by cells of the T lymphoid lineage to its corresponding arabinosylguanine nucleotide triphosphate (araGTP), resulting in inhibition of DNA synthesis and selective in vitro toxicity to T lymphoblastoid cell lines as well as to freshly isolated leukemia cells from patients with T cell acute lymphoblastic leukemia (ALL).

Ara-G induced an S-phase arrest in both Raji and ML-1. Within 3 hours of Ara-G treatment, the levels of soluble Fas ligand (sFasL) in the medium increased significantly in CEM cultures. Pretreatment of CEM cells with a Fas antagonistic antibody inhibited ara-G-mediated cell death[3].

Intravenous injection of 10(6) 6C3HED cells resulted in 100 percent mortality within 18 days, with autopsy revealing tumor infiltration of multiple organs. Evidence of araG's ability to purge bone marrow of malignant tumor cells without causing significant toxicity to normal marrow-derived hematopoietic progenitor cells was documented in experiments in which 75 percent of lethally irradiated mice receiving transplants of syngeneic bone marrow contaminated with 6C3HED tumor cells and treated ex vivo with 100 mM araG for 18 hours survived for 250 to >400 days. Reconstitution of the lymphoid, myeloid, and erythroid lineages with donor cells in surviving mice was documented. The data presented indicate that araG may effectively purge bone marrow of malignant T cells without irreversible toxicity to hematopoietic stem cells[1].

38819-10-2

C10H13N5O5

283.24

DMSO:5 mg/mL
Ethanol:Partially Soluble
DMF:3 mg/mL
PBS (pH 7.2):0.3 mg/mL
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In solvent: -80°C for 2 years