A Limited-Center, Prospective, Double-Blind, Placebo-Controlled Study to Evaluate the Effects of Cenicriviroc Mesylate on Arterial Inflammation in People Living With HIV

The study is being conducted to determine if cenicriviroc mesylate (CVC) will decrease vascular inflammation as measured by 18F-fluorodeoxyglucose (FDG)-positron emission tomography (PET)/computed tomography (CT) imaging of the aorta.

Start Date30 May 2023

Sponsor / Collaborator

National Institute of Allergy & Infectious Diseases

[+1]

NCT04334915

/ WithdrawnPhase 2IIT

A Multicenter, Prospective, Double-Blind, Placebo-Controlled Study to Evaluate the Effects of Cenicriviroc Mesylate on Arterial Inflammation in People Living With HIV

The purpose of this study is to evaluate the effects of cenicriviroc mesylate (CVC) on arterial inflammation in people living with HIV.

Start Date22 Nov 2022

Sponsor / Collaborator

National Institute of Allergy & Infectious Diseases

[+1]

NCT04593940

/ CompletedPhase 3IIT

Randomized Master Protocol for Immune Modulators for Treating COVID-19

ACTIV-1 IM is a master protocol designed to evaluate multiple investigational agents for the treatment of moderately or severely ill patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The research objectives are to evaluate each agent with respect to speed of recovery, mortality, illness severity, and hospital resource utilization. Each agent will be evaluated as add-on therapy to the standard of care (SoC) in use at the local clinics, including remdesivir (provided). The SoC may change during the course of the study based on other research findings. Comparisons of the agents among themselves is not a research objective.
The study population corresponds to moderately and severely ill patients infected with the coronavirus disease 2019 (COVID-19) virus. Recruitment will target patients already hospitalized for treatment of COVID-19 infection as well as patients being treated for COVID-19 infection in Emergency Departments while waiting to be admitted to the hospital. Patients both in and out of the ICU are included in the study population.

Start Date15 Oct 2020

Sponsor / Collaborator

Duke University

[+2]

100 Clinical Results associated with Cenicriviroc mesylate

100 Translational Medicine associated with Cenicriviroc mesylate

100 Patents (Medical) associated with Cenicriviroc mesylate

364

Literatures (Medical) associated with Cenicriviroc mesylate

01 Feb 2025·Journal of Orthopaedic Research

Pharmacological antagonism of Ccr2+ cell recruitment to facilitate regenerative tendon healing

Article

Author: Loiselle, Alayna E. ; Rodenhouse, Andrew ; Ketonis, Constantinos ; Smolyak, Gilbert ; Nichols, Anne E. C.

AbstractSuccessful tendon healing requires sufficient deposition and remodeling of new extracellular matrix at the site of injury, with this process mediating in part through fibroblast activation via communication with macrophages. Moreover, resolution of healing requires clearance or reversion of activated cells, with chronic interactions with persistent macrophages impairing resolution and facilitating the conversion to fibrotic healing. As such, modulation of the macrophage environment represents an important translational target to improve the tendon healing process. Circulating monocytes are recruited to sites of tissue injury, including the tendon, via upregulation of cytokines including Ccl2, which facilitates recruitment of Ccr2+ macrophages to the healing tendon. Our prior work has demonstrated that Ccr2−/− can modulate fibroblast activation and myofibroblast differentiation. However, this approach lacked temporal control and resulted in healing impairments. Thus, in the current study we have leveraged a Ccr2 antagonist to blunt macrophage recruitment to the healing tendon in a time‐dependent manner. We first tested the effects of Ccr2 antagonism during the acute inflammatory phase and found that this had no effect on the healing process. In contrast, Ccr2 antagonism during the early proliferative/granulation tissue period resulted in significant improvements in mechanical properties of the healing tendon. Collectively, these data demonstrate the temporally distinct impacts of modulating Ccr2+ cell recruitment and Ccr2 antagonism during tendon healing and highlight the translational potential of transient Ccr2 antagonism to improve the tendon healing process.

01 Jan 2025·International Immunopharmacology

Inhibition of CCR2 attenuates NLRP3-dependent pyroptosis after myocardial ischaemia–reperfusion in rats via the NF-kB pathway

Article

Author: Wang, Yun ; Xie, Jun ; Cheng, Xueying ; Dou, Mengyun ; Ge, Jinlong ; Ma, Lan ; Chen, Xinran

Myocardial infarction (MI) is a leading cause of mortality worldwide, contributing significantly to long-term cardiac dysfunction and heart failure. Effective therapeutic strategies are urgently needed to mitigate the extensive damage caused by MI and subsequent ischemia-reperfusion (I/R) injury. This study investigates the role of the Chemokine receptor 2 (CCR2) in regulating NLRP3-dependent cardiomyocyte pyroptosis following myocardial ischemia-reperfusion (MIR), elucidating its molecular mechanisms. A myocardial ischemia-reperfusion model was established using 124 Sprague-Dawley rats by ligating the left coronary artery, inducing 30 min of ischemia. Following ischemia, RS504393, a selective CCR2 antagonist, was administered intraperitoneally one hour after reperfusion. To further explore the underlying mechanisms, the NF-κB pathway agonist Phorbol 12-myristate 13-acetate (PMA) was administered 1 h post-MIR. The results showed a marked increase in CCR2 expression in the heart, peaking on the first day of reperfusion. Treatment with RS504393 significantly improved short-term cardiac function and reduced myocardial infarction size, decreased myocardial pyroptosis and suppressed the expression of NLRP3, GSDMD, Caspase-1, IL-1β, and IL-18 through inhibition of the NF-κB signaling pathway. This effect was reversed with the administration of PMA. In summary, the inhibition of CCR2 shows potential in mitigating myocardial injury following MIR by modulating the NF-κB signaling pathway. These findings highlight CCR2 as a promising therapeutic target for myocardial ischemia-reperfusion injury.

01 Dec 2024·Journal of Theoretical Biology

Optimal control of combination immunotherapy for a virtual murine cohort in a glioblastoma-immune dynamics model

Article

Author: Takacs, Gregory P. ; Anderson, Hannah G ; Takacs, Gregory P ; Harrison, Jeffrey K ; Stepien, Tracy L. ; Anderson, Hannah G. ; Harrison, Jeffrey K. ; Rong, Libin ; Stepien, Tracy L

The immune checkpoint inhibitor anti-PD-1, commonly used in cancer immunotherapy, has not been successful as a monotherapy for the highly aggressive brain cancer glioblastoma. However, when used in conjunction with a CC-chemokine receptor-2 (CCR2) antagonist, anti-PD-1 has shown efficacy in preclinical studies. In this paper, we aim to optimize treatment regimens for this combination immunotherapy using optimal control theory. We extend a treatment-free glioblastoma-immune dynamics ODE model to include interventions with anti-PD-1 and the CCR2 antagonist. An optimized regimen increases the survival of an average mouse from 32 days post-tumor implantation without treatment to 111 days with treatment. We scale this approach to a virtual murine cohort to evaluate mortality and quality of life concerns during treatment, and predict survival, tumor recurrence, or death after treatment. A parameter identifiability analysis identifies five parameters suitable for personalizing treatment within the virtual cohort. Sampling from these five practically identifiable parameters for the virtual murine cohort reveals that personalized, optimized regimens enhance survival: 84% of the virtual mice survive to day 100, compared to 60% survival in a previously studied experimental regimen. Subjects with high tumor growth rates and low T cell kill rates are identified as more likely to die during and after treatment due to their compromised immune systems and more aggressive tumors. Notably, the MDSC death rate emerges as a long-term predictor of either disease-free survival or death.

News (Medical) associated with Cenicriviroc mesylate

11 Jul 2023

·www.pharmaceutical-technology.com

Covid-19: Anti-inflammatory drugs do not lead to a swifter hospital exit

Robert Barrie There were still over 6,000 hospitalisations due to Covid-19 in the past week in the US. Unvaccinated adults are fives times more likely to die from the disease. Image credit: Shutterstock/Gorodenkoff Anti-inflammatory drugs may reduce deaths due to Covid-19, but they do not help speed up the recovery for those in hospital, according to a recent study. Results from the study , published in The Journal of the American Medical Association , demonstrated that giving abatacept , cenicriviroc, or Johnson and Johnson’s Remicade (infliximab) in addition to standard of care did not decrease time to recovery for patients hospitalised with Covid-19 pneumonia. The standard of care included in this study involved Gilead Sciences’ Veklury (remdesivir) and the corticosteroid dexamethasone. Recommended Reports Reports Artificial Intelligence in Healthcare: Non-Invasive Physiological Monitoring GlobalData Reports Nitric Oxide Synthase (NO Synthase or NOS or EC 1.14.13.39) Drugs in Development by Therapy Areas... GlobalData View all Companies Intelligence SOC Co., Ltd Roche S.A. Genentech, Inc. JAMA Sp. z o.o. View all Patients who took either one of the three drugs recovered after a similar number of days compared to those who were on placebo. The investigators also measured mortality across the sub-studies by day 28 – which did show slight differences, though not statistically significant. Abatacept and Remicade led to a narrow decrease in patient deaths – a 4.1% and 4.4% difference respectively, whilst the cenicriviroc group’s mortality rose by 1.9%. A limitation with the latter group was adherence, however, as cenicriviroc is orally administered, unlike abatacept and Remicade which are infused intravenously. Though the study did not meet any endpoints, the authors note that “expanding treatment armament” is important as SARS-CoV-2 variants may always emerge that may evade antiviral treatments. Although the World Health Organization (WHO) declared an end to the Covid-19 public health emergency, there were still over 6,000 hospitalisations due to the disease in the past week in the US. Based on statistics from March 2023, the Centers for Disease Control and Prevention state that unvaccinated adults are around five times more likely to die from Covid-19. The JAMA trial remains a helpful scaffold with the investigators saying that other previous large-scale Covid-19 studies have not concurrently evaluated multiple agents whilst simultaneously providing a shared placebo group. Still, the study was a randomised, double-masked, placebo-controlled clinical trial (NCT04593940) that enrolled almost 2,000 patients, in comparison to other smaller open-label studies that explored similar questions. However, a limitation of this study itself was that it took place before the SARS-CoV-2 Omicron variant became prevalent. During the pandemic, Covid-19 patients were prescribed the corticosteroid dexamethasone, with research showing that the drug reduces mortality for patients on respiratory support. There was interest in whether giving additional, targeted anti-inflammatory agents could complement steroid action. Tocilizumab, marketed as Actemra by Roche subsidiary Genentech, was given emergency authorisation by the US Food and Drug Administration (FDA) for treating hospitalised Covid-19 patients receiving systemic corticosteroids. “One of the fundamental questions of early Covid-19 research was whether we could dampen the inflammatory process using existing anti-inflammatory drugs,” said Dr. William G. Powderly, national principal investigator of the trial. “Our data suggest that two of the drugs we studied can be given to reduce mortality in severely ill patients. We hope this study will be helpful in revising guidelines for best practices in treating patients hospitalized with Covid-19.”

Clinical StudyClinical ResultDrug Approval

26 Jun 2023

·www.prnewswire.com

Ascletis Announces Poster Presentation of Phase II Study of ASC42 FXR Agonist for Functional Cure of Chronic Hepatitis B at EASL CONGRESS 2023

HANGZHOU and SHAOXING, China, June 25, 2023 /PRNewswire/ -- Ascletis Pharma Inc. (HKEX:1672, "Ascletis") today announces the poster presentation of ASC42, a novel farnesoid X receptor (FXR) agonist, in combination with PEGylated interferon (PEG-IFN) and entecavir (ETV) in chronic hepatitis B (CHB) patients with 12-week treatment at European Association for the Study of the Liver (EASL) CONGRESS 2023. The summary of the abstract is shown as below: Title: A phase 2 study of ASC42, a novel farnesoid X receptor (FXR) agonist, in combination with PEGylated interferon (PEG-IFN) and entecavir (ETV) in chronic hepatitis B patients with 12-week treatment Presenter: Jinzi J. Wu, Ph.D. Principal Investigator: Prof. Jinlin Hou, Nanfang Hospital of Southern Medical University Poster Number: SAT-201 Category: Viral Hepatitis B and D Study Design: This Phase 2 trial (NCT05107778) was a multi-center, randomized, single-blind, placebo-controlled study conducted in China. Forty-three HBeAg negative, hepatitis B virus (HBV) DNA Results: In total, 122, 119, and 107 adverse events (AEs) were reported in 10 mg ASC42, 15 mg ASC42 and PBO cohorts, respectively, and most AEs (94.3%) were mild (grade 1) or moderate (grade 2) in severity. One subject in 15 mg ASC42 cohort experienced a grade 3 serious AE (SAE) of liver function injury with a final outcome of recovered. Pruritus is the most common AE, and study drug-related pruritus was reported in 1 (6.7%), 7 (50%) and 0 (0%) subjects in 10 mg ASC42, 15 mg ASC42 and PBO cohorts, respectively. Pruritus rate of 10 mg ASC42 (6.7%) is lower than other FXR agonists in non-alcoholic steatohepatitis (NASH) patients. Conclusion: In CHB patients, 12-week treatment of 10 mg ASC42 in combination of PEG-IFN-α-2a and ETV was safe and well-tolerated and showed minimum and mild pruritus (6.7%). Previous study indicated that in healthy subjects, 14-day treatment of ASC42 alone demonstrated 471%~1,780% increase of fibroblast growth factor 19 (FGF19) and 53%~91% decrease of 7α-hydroxy-4-cholesten-3-one (C4) at a dose range of 5 mg~15 mg. Data suggest that at the therapeutic dose of 10 mg, the novel FXR agonist ASC42 is differentiated from other FXR agonists in terms of pruritus. [1]. Data on file [2]. Younossi Z.M., Ratziu V., Loomba R., et al. Obeticholic acid for the treatment of non-alcoholic steatohepatitis: interim analysis from a multicentre, randomised, placebo-controlled phase 3 trial [J]. The Lancet, 2019, 394(10215): 2184-96.DOI: 10.1016/s0140-6736(19)33041-7 [3]. Lau G.K., Piratvisuth T., Luo K.X., et al. Peginterferon Alfa-2a, lamivudine, and the combination for HBeAg-positive chronic hepatitis B [J]. N Engl J Med, 2005, 352(26): 2682-95.DOI: 10.1056/NEJMoa043470 [4]. Loomba R., Noureddin M., Kowdley K.V., et al. Combination Therapies Including Cilofexor and Firsocostat for Bridging Fibrosis and Cirrhosis Attributable to NASH [J]. Hepatology, 2021, 73(2): 625-43.DOI: 10.1002/hep.31622 [5]. Anstee Q.M., Lucas K.J., Francque S., et al. Tropifexor plus cenicriviroc combination versus monotherapy in non-alcoholic steatohepatitis: Results from the Phase 2b TANDEM study [J]. Hepatology, 2023.DOI: 10.1097/hep.0000000000000439 About EASL EASL, the European Association for the Study of the Liver, founded in 1966, is a medical association dedicated to pursuing excellence in liver research, to the clinical practice of liver disorders, and to providing education to all those interested in hepatology. As of 2022, EASL serves 4,900 members from 112 countries. About Ascletis Ascletis is an innovative R&D driven biotech listed on the Hong Kong Stock Exchange (1672.HK), covering the entire value chain from discovery and development to manufacturing and commercialization. Led by a management team with deep expertise and a proven track record, Ascletis focuses on three therapeutic areas with unmet medical needs from a global perspective: viral diseases, non-alcoholic steatohepatitis (NASH) and oncology. Through excellent execution, Ascletis rapidly advances its drug pipeline with an aim of leading in global competition. To date, Ascletis has three marketed products, i.e. ritonavir tablets, GANOVO® and ASCLEVIR®, and 23 drug candidates in its R&D pipeline. The most advanced drug candidates include ASC22 (HBV functional cure), ASC10 and ASC11(oral small molecules for COVID-19 treatment), ASC40 (recurrent glioblastoma), ASC42 (PBC, primary biliary cholangitis), and ASC40 (acne). For more information, please visit . SOURCE Ascletis Pharma Inc.

Clinical ResultPhase 2Phase 3

02 May 2023

·www.prnewswire.com

Viscient Biosciences Announces First Drug Discovered in 3D Bioprinted Models

Company's NASH Drug Expected to Enter Clinic in 2024 SAN DIEGO, May 2, 2023 /PRNewswire/ -- Viscient Bio, Inc. ("Viscient") today announced it has identified the world's first drug candidate discovered primarily using 3D bioprinted tissue models of disease formed from human cells. Viscient expects to develop the drug to treat non-alcoholic steatohepatitis (NASH), a growing epidemic disease that is believed to affect more than 10% of the US population. NASH can often lead to hepatocellular carcinoma or liver failure. Due to the devastating effects of NASH on patients and its wide prevalence, analysis have projected future pharma industry revenues for the drug in the tens of billions of dollars per year. Continue Reading Viscient's lead compound is an orally delivered small molecule designed to hit a novel target identified in 3D bioprinted and other 3D tissue models of disease. In preclinical studies, the drug has proven to be well tolerated. In Viscient's models of disease, the compound shows reduction of fibrosis as measured by histological evidence similar to that used for human liver biopsy. Using the same model, fibrosis reduction is also seen for obeticholic acid and resmetirom, while no fibrosis reduction is seen for drugs such as cenicriviroc, selonsertib, and elafibranor. The newly discovered target is predominantly expressed in liver tissue. Failed NASH drugs never would have been put in humans based on what can be clearly seen in these models. Tweet this "It is long past time to displace the model of drug development reliant on proof of activity in animals," said Viscient chief executive officer Keith Murphy. "Viscient's trailblazing work has resulted in 3d cellular human models of disease in which the performance of previously tested compounds has matched clinical results. Failed NASH drugs never would have been put in humans based on what can be clearly seen in these models. Our novel compound shows fibrosis reduction in these models, as do NASH drugs known to work in Phase 3, and we are excited to move this lead program forward." The lead compound's clear reduction of fibrosis in Viscient's NASH models is promising because Viscient's 3D models of NASH have shown extremely high correlation with clinical results in patients. The model demonstrates fibrosis reduction for known clinical compounds tested by pharma companies that have that effect in humans, while revealing lack of fibrosis reduction for compounds that failed in Phase 2 or Phase 3 for NASH. The model is accurate in predicting both successes and failures among clinical compounds tested to date. The gene expression of Viscient's models is also well correlated with that seen in disease samples from patients. Though tested post-hoc, the results are not backfit, as the model was finalized before testing of any clinical compounds was conducted. According to the Biotechnology Innovation Organization's 2021 report, only 7.9% of drugs that enter clinical trials are approved for human use. Viscient Biosciences believes that we can achieve a significantly better clinical translation rate than that using more relevant 3D human tissue models of disease, leading to more successes and lower drug development costs per approved drug. Viscient is leading the world in creation of human tissue models with accurate disease relevance, and demonstrating the application of these models to drug development at every stage. About Viscient Biosciences Viscient Biosciences is an early-stage biotechnology company that is developing novel therapies for NASH and other liver diseases. Its lead compound, built to a novel target discovered in proprietary 3D models of human liver disease, is expected to enter the clinic in 2024. Viscient's 3D models of NASH have shown extremely high correlation with clinical results in patients, demonstrating fibrosis reduction for compounds that have that effect in humans while revealing lack of fibrosis reduction for compounds that failed in Phase 2 or Phase 3 for NASH. The gene expression of Viscient's models is also well correlated with that seen in disease samples from patients. Utilizing these 3D human tissues as dynamic models of healthy and diseased human biology for drug development, the company identifies opportunities both for novel therapeutic development and the in-licensing and repurposing of drugs. SOURCE Viscient Bio, Inc.

Clinical Result

100 Deals associated with Cenicriviroc mesylate

External Link

KEGG	Wiki	ATC	Drug Bank
D09879	Cenicriviroc mesylate	-	DB11758

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Obesity	Phase 3	-	Tobira Therapeutics, Inc.	-
Obesity	Phase 3	-	Takeda Pharmaceutical Co., Ltd.	-
Fibrosis, Liver	Discovery	AU	Tobira Therapeutics, Inc.	05 Apr 2017
Fibrosis, Liver	Discovery	SG	Tobira Therapeutics, Inc.	05 Apr 2017
Fibrosis, Liver	Discovery	NO	Tobira Therapeutics, Inc.	05 Apr 2017
Fibrosis, Liver	Discovery	NZ	Tobira Therapeutics, Inc.	05 Apr 2017
Fibrosis, Liver	Discovery	GB	Tobira Therapeutics, Inc.	05 Apr 2017
Fibrosis, Liver	Discovery	HK	Tobira Therapeutics, Inc.	05 Apr 2017
Fibrosis, Liver	Discovery	TW	Tobira Therapeutics, Inc.	05 Apr 2017
Fibrosis, Liver	Discovery	PR	Tobira Therapeutics, Inc.	05 Apr 2017

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04593940 (Pubmed \| JAMA)	Phase 3	COVID-19	1,971	Abatacept	pagwqxselu(kclyyhegec) = cxwxtfnbcg uvjltdifwg (sakjlnszwp )	-	10 Jul 2023
				Cenicriviroc	pagwqxselu(kclyyhegec) = eqjvavgacj uvjltdifwg (sakjlnszwp )
NCT04593940 (ACTIV-1 IM, CTgov)	Phase 3	COVID-19	1,971	Infliximab (Standard of Care + Infliximab)	fvndtzqaji(qglmiakayd) = rfhxdwoqvs oofiziwdkj (nwjubjphqm, itmyaehssm - aqcmnpeets) View more	-	21 Apr 2023
				Placebo (Standard of Care + Infliximab Matching Placebo)	fvndtzqaji(qglmiakayd) = pbnhiyldob oofiziwdkj (nwjubjphqm, htjelrpaml - mnyrzsuoio) View more
NCT03028740 (AURORA, Pubmed)	Phase 3	Nonalcoholic Steatohepatitis	1,778	Cenicriviroc 150 mg	(huryuflwhr): odds ratio = 0.84 (95% CI, 0.63 - 1.1)	Negative	13 Apr 2023
				Placebo
NCT03028740 (AURORA, CTgov)	Phase 3	Fibrosis, Liver \| Nonalcoholic Steatohepatitis	1,778	Placebo (Placebo)	stuubuiwmn(ykqyqisguu) = gcjyacovnz gmufplzdes (wrhhjgtkht, vkcpajppzw - aedjwccyrs) View more	-	10 Mar 2022
				Cenicriviroc (Cenicriviroc 150 mg)	stuubuiwmn(ykqyqisguu) = stbqxokjvd gmufplzdes (wrhhjgtkht, cvzxscyiro - idolqcszog) View more
NCT03059446 (CTgov)	Phase 2	Fibrosis, Liver \| Nonalcoholic Steatohepatitis \| Liver Cirrhosis	167	Cenicriviroc	tjuhmvohzg(xdfzdaizxx) = urufakgmuj acldlbiwhl (zjracurnpd, cikcdkvmad - kpocxltzmt) View more	-	02 Feb 2022
NCT02653625 (PERSEUS, Pubmed \| Hepatol Commun) Manual	Phase 2	Cholangitis, Sclerosing	20	cenicriviroc	(mpbpelwnar) = zyobmyzunx oehrmldtdt (srekjdqnaz ) View more	Positive	22 Dec 2020
NCT02128828 (H020, CTgov)	Phase 2	Cognitive Dysfunction \| AIDS Dementia Complex	20	cenicriviroc	vatkotbdtv(lpjoihfbgk) = xvukmobhem wcljzffhoe (uvkpejjjxy, cybrquxvwp - cprohhrnsw) View more	-	20 Aug 2020
NCT02330549 (CTgov)	Phase 2	Diabetes Mellitus, Type 2 \| Prediabetic State \| Metabolic dysfunction-associated steatotic liver disease	45	Cenicriviroc 150 mg (Cenicriviroc 150 mg)	qhthroskvh(vwpojseeza) = pcguouhezl ucezzkjwzv (sqyfvevbhy, rixxwzysnm - marwhywhps) View more	-	11 Oct 2019
				Placebo (Placebo)	qhthroskvh(vwpojseeza) = vtyhtgrheq ucezzkjwzv (sqyfvevbhy, hvyogcvefo - uwhjhktnyz) View more
NCT02217475 (CENTAUR, EASD2019)	Phase 2	Nonalcoholic Steatohepatitis high-sensitivity C-reactive protein \| fibrinogen \| interleukin (IL)-6 ... View more	289	Cenicriviroc 150 mg	kvjjbdmjwa(sgfvcexkgk) = adverse events were comparable for CVC and placebo; no deaths occurred phsnksgggo (obubhdacgz )	Positive	19 Sep 2019
				Placebo
NCT02217475 (CENTAUR, ADA2019)	Not Applicable	Nonalcoholic Steatohepatitis	289	Cenicriviroc 150 mg	jbpmzxsajd(ijugyzovjo) = ypmcmnbxkz nbjwkpwwsm (akvftxkcdn )	-	01 Jun 2019
				Placebo	jbpmzxsajd(ijugyzovjo) = rnudnuvtny nbjwkpwwsm (akvftxkcdn )

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