Fiume L, Bassi B, Busi C, Mattioli A, Spinosa G
Biochem Pharmacol. 1986 Mar 15;35(6):967-72. doi: 10.1016/0006-2952(86)90084-5.
With the aim of improving the chemotherapeutic index of 9-beta-D-arabinofuranosyl-adenine 5' monophosphate (ara-AMP) in the treatment of chronic hepatitis B, this drug was conjugated with lactosaminated serum albumin (L-SA), a neoglycoprotein which only enters into hepatocytes. We used a L-SA-ara-AMP conjugate which, in contrast to those previously employed, has the advantage of remaining soluble after lyophilization. We found in mice that: (I) this new conjugate was quite stable in the bloodstream where only a small part of ara-AMP was released; (II) after administration of the conjugate labelled in the drug moiety both acid insoluble and soluble radioactivities were several times higher in liver than in other organs; (III) in mice with Ectromelia virus hepatitis, the conjugate inhibited virus DNA synthesis in liver without affecting cellular DNA synthesis in intestine and bone marrow; (IV) the conjugate did not display any recognizable sign of acute toxicity even at doses several fold higher than those pharmacologically active; and (V) when prepared with homologous albumin it was not immunogenic.
为提高9-β-D-阿拉伯呋喃糖基腺嘌呤5′-单磷酸酯(ara-AMP)治疗慢性乙型肝炎的化疗指数,将该药物与乳糖胺化血清白蛋白(L-SA)偶联,L-SA是一种仅进入肝细胞的新糖蛋白。我们使用了一种L-SA-ara-AMP偶联物,与先前使用的偶联物相比,它具有冻干后仍保持可溶的优点。我们在小鼠中发现:(I)这种新偶联物在血流中相当稳定,只有一小部分ara-AMP被释放;(II)给予药物部分标记的偶联物后,肝脏中的酸不溶性和可溶性放射性比其他器官高几倍;(III)在感染埃可病毒肝炎的小鼠中,偶联物抑制肝脏中的病毒DNA合成,而不影响肠道和骨髓中的细胞DNA合成;(IV)即使在比药理活性剂量高几倍的剂量下,偶联物也没有表现出任何明显的急性毒性迹象;(V)当用同源白蛋白制备时,它没有免疫原性。