Scozzafava Andrea, Mastrolorenzo Antonio, Supuran Claudiu T
Università degli Studi di Firenze, Dipartimento di Chimica, Italy.
J Enzyme Inhib Med Chem. 2002 Apr;17(2):69-76. doi: 10.1080/14756360290024227.
HIV entry within the cell involves the presence of at least two chemokine co-receptors, the CCR5 and CXCR4 receptors. Viral entry can be inhibited by the natural ligands for CXCR4, the CXC chemokine SDF-1 and CCR5, the CC chemokines RANTES, MIP-1alpha and MIP-1beta, respectively. Much research has been devoted ultimately to the development of small molecule chemokine antagonists that inhibit virus entry within the cell, and constitute in this way novel antiviral medications. The most potent and specific CXCR4 antagonists reported up to now are the bicyclam derivatives, which also potently block X4 HIV replication. One such compound, AMD3100 has proved to be a highly specific CXCR4 antagonist, which consistently blocks the outgrowth of all X4 HIV and dual-tropic (R5/X4) variants that use CXCR4 for entering the cells. From such bicyclam analogues, AMD3100 was selected as the clinical candidate, which, after initial Phase I studies, proceeded to Phase II trials, but unfortunately showed significant cardiac side effects which lead to its withdrawal from further development. The first nonpeptidic compound that interacts with CCR5, but not with CXCR4, is a quaternary ammonium derivative, TAK-779, which also shows potent but variable anti-HIV activity. A large number of potent CCR5 antagonists from several classes of polycyclic derivatives have been recently disclosed. Many such derivatives showed nanomolar binding affinity to the receptor, and at least one of them, the oxime-piperidine derivative SCH-351125 has progressed to clinical evaluation. The development of such agents for clinical use may constitute an additional approach for the treatment of HIV infection, in addition to the classical one involving reverse transcriptase and protease inhibitors.
HIV进入细胞需要至少两种趋化因子共受体,即CCR5和CXCR4受体。病毒进入可分别被CXCR4的天然配体CXC趋化因子SDF-1以及CCR5的天然配体CC趋化因子RANTES、MIP-1α和MIP-1β所抑制。许多研究最终致力于开发抑制病毒进入细胞的小分子趋化因子拮抗剂,从而构成新型抗病毒药物。目前报道的最有效且特异的CXCR4拮抗剂是双环胺衍生物,它们也能有效阻断X4型HIV复制。一种这样的化合物AMD3100已被证明是高度特异的CXCR4拮抗剂,它能持续阻断所有利用CXCR4进入细胞的X4型HIV和双嗜性(R5/X4)变体的生长。从这类双环胺类似物中,AMD3100被选为临床候选药物,在最初的I期研究后进入II期试验,但不幸的是显示出显著的心脏副作用,导致其停止进一步开发。首个与CCR5相互作用但不与CXCR4相互作用的非肽类化合物是季铵衍生物TAK-779,它也显示出强效但不稳定的抗HIV活性。最近已公开了几类多环衍生物中的大量强效CCR5拮抗剂。许多这类衍生物对该受体显示出纳摩尔级的结合亲和力,其中至少一种肟-哌啶衍生物SCH-351125已进入临床评估阶段。除了涉及逆转录酶和蛋白酶抑制剂的传统方法外,开发这类临床用药可能为治疗HIV感染提供另一种途径。