 | |
| Names | |
|---|---|
| Preferred IUPAC name (5E)-8-[4-(2-Butoxyethoxy)phenyl]-1-(2-methylpropyl)-N-{4-[(S)-(1-propyl-1H-imidazol-5-yl)methanesulfinyl]phenyl}-1,2,3,4-tetrahydro-1-benzazocine-5-carboxamide | |
| Other names TAK-652; TBR-652 | |
| Identifiers | |
3D model (JSmol) | |
| ChEBI | |
| ChEMBL | |
| ChemSpider | |
| KEGG | |
PubChem CID | |
| UNII | |
CompTox Dashboard (EPA) | |
| |
| |
| Properties | |
| C41H52N4O4S | |
| Molar mass | 696.95 g·mol−1 |
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa). | |
Cenicriviroc (INN, [1] code names TAK-652, TBR-652, commonly abbreviated as CVC) is an experimental drug candidate for the treatment of HIV infection [2] and in combination with Tropifexor for non-alcoholic steatohepatitis. [3] It is being developed by Takeda and Tobira Therapeutics.[ citation needed ]
Cenicriviroc is an inhibitor of CCR2 and CCR5 receptors, [4] allowing it to function as an entry inhibitor which prevents the virus from entering into a human cell. Inhibition of CCR2 may have an anti-inflammatory effect.[ citation needed ]
A double-blind, randomized, placebo-controlled clinical study to assess the antiviral activity, safety, and tolerability of cenicriviroc was conducted in 2010. HIV-infected patients taking cenicriviroc had significant reductions in viral load, with the effect persisting up to two weeks after discontinuation of treatment. [5] Additional Phase II clinical trials are underway. [6] [ when? ]
Cenicriviroc is also in two separate clinical trials for COVID-19: the ACTIV-I trial run by the National Center for Advancing Translational Sciences, where it is compared with a number of other immunomodulatory agents, [7] and the Charité Trial of Cenicriviroc at the Charité Hospital in Berlin. [8] As of 2 July 2021 [update] , both trials are recruiting participants, and are expected to complete in September 2021.[ citation needed ]
Phase IIb data presented at the 20th Conference on Retroviruses and Opportunistic Infections (CROI) in March 2013 showed similar viral suppression rates of 76% for patients taking 100 mg cenicriviroc, 73% with 200 mg cenicriviroc, and 71% with efavirenz. Non-response rates were higher with cenicriviroc, however, largely due to greater drop-out of patients. A new tablet formulation with lower pill burden may improve adherence. Looking at immune and inflammatory biomarkers, levels of MCP-1 increased and soluble CD14 decreased in the cenicriviroc arms. [9]