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SYN-004的研发,一种口服β-内酰胺酶治疗药物,用于保护肠道微生物群免受抗生素介导的损害并预防艰难梭菌感染。

Development of SYN-004, an oral beta-lactamase treatment to protect the gut microbiome from antibiotic-mediated damage and prevent Clostridium difficile infection.

作者信息

Kaleko Michael, Bristol J Andrew, Hubert Steven, Parsley Todd, Widmer Giovanni, Tzipori Saul, Subramanian Poorani, Hasan Nur, Koski Perrti, Kokai-Kun John, Sliman Joseph, Jones Annie, Connelly Sheila

机构信息

Synthetic Biologics, Inc., Rockville, MD, USA.

Synthetic Biologics, Inc., Rockville, MD, USA.

出版信息

Anaerobe. 2016 Oct;41:58-67. doi: 10.1016/j.anaerobe.2016.05.015. Epub 2016 Jun 2.

Abstract

The gut microbiome, composed of the microflora that inhabit the gastrointestinal tract and their genomes, make up a complex ecosystem that can be disrupted by antibiotic use. The ensuing dysbiosis is conducive to the emergence of opportunistic pathogens such as Clostridium difficile. A novel approach to protect the microbiome from antibiotic-mediated dysbiosis is the use of beta-lactamase enzymes to degrade residual antibiotics in the gastrointestinal tract before the microflora are harmed. Here we present the preclinical development and early clinical studies of the beta-lactamase enzymes, P3A, currently referred to as SYN-004, and its precursor, P1A. Both P1A and SYN-004 were designed as orally-delivered, non-systemically available therapeutics for use with intravenous beta-lactam antibiotics. SYN-004 was engineered from P1A, a beta-lactamase isolated from Bacillus licheniformis, to broaden its antibiotic degradation profile. SYN-004 efficiently hydrolyses penicillins and cephalosporins, the most widely used IV beta-lactam antibiotics. In animal studies, SYN-004 degraded ceftriaxone in the GI tract of dogs and protected the microbiome of pigs from ceftriaxone-induced changes. Phase I clinical studies demonstrated SYN-004 safety and tolerability. Phase 2 studies are in progress to assess the utility of SYN-004 for the prevention of antibiotic-associated diarrhea and Clostridium difficile disease.

摘要

肠道微生物群由栖息在胃肠道的微生物群落及其基因组组成,构成了一个复杂的生态系统,抗生素的使用可能会破坏这个系统。随之而来的生态失调有利于艰难梭菌等机会性病原体的出现。一种保护微生物群免受抗生素介导的生态失调影响的新方法是使用β-内酰胺酶在微生物群落受到损害之前降解胃肠道中的残留抗生素。在此,我们介绍了β-内酰胺酶P3A(目前称为SYN-004)及其前体P1A的临床前开发和早期临床研究。P1A和SYN-004均被设计为口服给药、非全身可用的治疗药物,用于与静脉注射β-内酰胺抗生素联合使用。SYN-004是由从地衣芽孢杆菌中分离出的β-内酰胺酶P1A改造而来,以拓宽其抗生素降解谱。SYN-004能有效水解青霉素和头孢菌素,这是最广泛使用的静脉注射β-内酰胺抗生素。在动物研究中,SYN-004在犬胃肠道中降解头孢曲松,并保护猪的微生物群免受头孢曲松诱导的变化影响。I期临床研究证明了SYN-004的安全性和耐受性。目前正在进行2期研究,以评估SYN-004在预防抗生素相关性腹泻和艰难梭菌病方面的效用。

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