Background; A new mouth rinse formulation ("Lacer Oros Acción Integral", Lacer SA, Barcelona, Spain) has been recently proposed, including O-Cymen-5-ol, potassium nitrate, zinc chloride, dipotassium glycyrrhizate, sodium fluoride, panthenol and xylitol, within its ingredients. Thus, it may be relevant to test the efficacy of this new "Lacer Oros Acción Integral" mouth rinse formulation in a RCT.
Primary Objective: The primary objective of this RCT will be to evaluate the antiplaque/antigingivitis effects of the test mouth rinse.
Population: Consecutive subjects in supportive periodontal therapy (SPT) will be screened at the Post-Graduate Periodontal Clinic in the University Complutense, Madrid, and enrolled in the clinical trial if they are periodontitis patients, already enrolled in a SPT, for at least 6 months, systemically healthy, with moderate gingival inflammation and complains of dentin hypersensitivity.
Study design: pilot, parallel, double-blind, randomized, placebo-controlled, 12-week, clinical trial
Intervention: The experimental group will use three times daily a provided manual toothbrush with a sodium fluoride dentifrice, followed by the use of the test mouth rinse (Lacer Oros Acción Integral - new formula, Barcelona, Spain). The control group will use three times daily a provided manual toothbrush with a sodium fluoride dentifrice, followed by the use of the control mouth rinse (Lacer Oros Acción Integral - new formula, without active ingredients, Barcelona, Spain).
Visits: Screening, baseline, 2 and 12 weeks.
Outcomes: Periodontal clinical outcomes (plaque levels, gingival condition, probing pocket depth), Stainign, Microbiological outcomes (culture and qPCR). Patient reported outcomes, compliance, adverse effects.

Start Date04 Sep 2021

Sponsor / Collaborator

Universidad Complutense de Madrid

[+1]

NCT04395950

/ WithdrawnPhase 1IIT

A Phase 1B, Single-Blinded, Linear Two Period, Placebo-controlled Study to Evaluate the Effects of 10 mg/Day of PF-05221304, Liver Targeted Acetyl-CoA Carboxylase Inhibitor (ACCi) on Very Low Density Lipoprotein ApoB100 and TG Secretion

The purpose of this study is to assess the effects of an investigational drug, PF-05221304 (PF'1304) on the way the liver handles fat. The planned study will identify why the fat in the blood increases at the same time this drug reduces fat in the liver. The study will have two treatment periods of 6 weeks each, separated by a 3 week rest period with no treatment. The subjects will receive the active drug in one of the 6 week treatment periods and a placebo in the other 6 week period. The investigators will know when the subjects are receiving active treatment or placebo, but the subject will not know.

Start Date01 Dec 2020

Sponsor / Collaborator

Columbia University

[+1]

NCT04399538

/ CompletedPhase 2

A PHASE 2A, 2-PART, RANDOMIZED, DOUBLE-BLIND, DOUBLE-DUMMY PLACEBO-CONTROLLED, PARALLEL-GROUP (SPONSOR OPEN) STUDY TO ASSESS PHARMACODYNAMICS AND SAFETY OF PF-06865571 (DGAT2I) COADMINISTERED WITH PF-05221304 (ACCI) IN ADULT PARTICIPANTS WITH PRESUMED NONALCOHOLIC STEATOHEPATITIS (NASH)

The study will evaluate the effect of coadministration of a range of doses of DGAT2i with 1 dose of ACCi, on hepatic steatosis and the ability of DGAT2i to mitigate ACCi-induced elevations in serum triglycerides. The study has a 2-part design with sequential conduct of Part 1 and Part 2 with each part conducted in distinct/separate cohorts of participants. The overall study design, objectives/endpoints, eligibility criteria for both parts is envisioned to be identical, however, data from Part 1 will be used to determine whether to conduct Part 2.

Start Date10 Aug 2020

Sponsor / Collaborator

Pfizer Inc.

100 Clinical Results associated with Clesacostat

100 Translational Medicine associated with Clesacostat

100 Patents (Medical) associated with Clesacostat

Literatures (Medical) associated with Clesacostat

01 Dec 2025·JOURNAL OF CLINICAL PHARMACOLOGY

Effect of Varying Degrees of Hepatic Impairment on the Pharmacokinetics of Ervogastat, a Diacylglycerol Acyltransferase 2 (DGAT2) Inhibitor, and Clesacostat, an Acetyl‐CoA Carboxylase (ACC) Inhibitor

Article

Author: Hughes, Jim ; Amin, Neeta B. ; Bergman, Arthur J. ; Gosset, James R. ; Vourvahis, Manoli ; Ogden, Adam G. ; Kalgutkar, Amit S.

Abstract:

Ervogastat, a diacylglycerol‐O‐acyltransferase‐2 inhibitor, and clesacostat, an acetyl‐CoA carboxylase inhibitor, are in clinical development for the treatment of metabolic dysfunction‐associated steatohepatitis (MASH). Study 1 and Study 2 were open‐label, Phase 1 trials that assessed the pharmacokinetics (PK) of a single dose of ervogastat (100 mg) and clesacostat (25 mg), respectively, in participants (n = 6/cohort) with mild, moderate, or severe hepatic impairment (HI) and compared to those without HI (reference). Plasma samples were analyzed for both total and unbound concentrations in Study 2 as clesacostat is highly protein bound. In Study 1, compared to participants without HI, ervogastat exposure (AUC inf ) was 56%, 65%, and 52% higher in participants with mild, moderate, and severe HI, respectively. However, when excluding PK data from a participant with unexplained low exposures in reference group, ervogastat exposures were similar between those with/without HI. In Study 2, total clesacostat exposure was 36%, 24%, and 19% higher for mild, moderate, and severe HI, respectively, as compared to reference group. Unbound clesacostat exposures were 70%, 83%, and 166% higher for mild, moderate, and severe HI cohorts, respectively, with clesacostat plasma protein binding shown to decrease with increasing HI severity. Ervogastat and clesacostat were well tolerated with no clinically significant laboratory abnormalities or changes in vital signs and/or electrocardiograms observed. Observed exposures in HI studies were consistent with simulated exposures in MASH population. Taking into consideration the safety margins at the highest doses evaluated in Phase 2, no dose adjustment of ervogastat or clesacostat is currently warranted for patients with hepatic impairment.

01 Oct 2025·The Lancet Gastroenterology & Hepatology

Efficacy and safety of ervogastat alone and in combination with clesacostat in patients with biopsy-confirmed metabolic dysfunction-associated steatohepatitis and F2–F3 fibrosis (MIRNA): results from a phase 2, randomised, double-blind, double-dummy study

Article

Author: Nakajima, Atsushi ; Takahashi, Hirokazu ; Charlton, Michael ; Alkhouri, Naim ; Darekar, Amanda ; Tacke, Frank ; Wong, Vincent Wai-Sun ; Anstee, Quentin M ; Amin, Neeta B ; Rodriguez, Hector ; Kiszko, Jan

BACKGROUND:

Ervogastat, a diacylglycerol acyltransferase 2 (DGAT2) inhibitor, and clesacostat, an acetyl-coenzyme A carboxylase (ACC) inhibitor, have shown promise in reducing hepatic steatosis. Increased circulating triglycerides, a mechanistic consequence of ACC inhibitors, has been shown to be downregulated by DGAT2 inhibitor co-administration. We assessed the efficacy and safety of ervogastat alone and ervogastat plus clesacostat in adults with biopsy-confirmed metabolic dysfunction-associated steatohepatitis (MASH) and fibrosis stage 2 or 3.

METHODS:

This phase 2 double-blind, double-dummy, randomised study was conducted at 198 clinical sites across 11 countries. A computer-generated randomisation code (random permuted blocks method) was used to allocate patients to treatment groups in equal ratios, and stratified based on degree of fibrosis (F2 vs F3), using an interactive response technology system to ervogastat (25 mg, 75 mg, 150 mg, or 300 mg), ervogastat plus clesacostat (150 mg plus 5 mg or 300 mg plus 10 mg), or placebo, twice daily for 48 weeks. The primary endpoint was the proportion of patients achieving MASH resolution without fibrosis worsening, at least 1 stage fibrosis improvement without MASH worsening, or both, at week 48. Patients were analysed according to the treatment group they were assigned to. The primary endpoint was analysed based on the full analysis set (all randomly assigned patients who took at least one dose of study treatment who provided evaluable baseline biopsy data) in which patients missing a week 48 biopsy were considered non-responders. This completed trial was registered with ClinicalTrials.gov (NCT04321031).

FINDINGS:

Recruitment began June 15, 2020; randomisation was completed Feb 22, 2023, with 255 patients randomly assigned and given treatment (73% of planned sample size; ervogastat 25 mg: N=35; ervogastat 75 mg: N=48; ervogastat 150 mg: N=42; ervogastat 300 mg: N=31; ervogastat 150 mg plus clesacostat 5 mg: N=35; ervogastat 300 mg plus clesacostat 10 mg: N=30; placebo: N=34). 13 (38%) patients in the placebo group achieved the composite primary endpoint, as did 16 (46%) in the ervogastat 25 mg group (difference from placebo in the proportion of patients achieving the primary endpoint 0·08 [90% CI -0·11 to 0·27]), 25 (52%) in the ervogastat 75 mg group (0·14 [-0·04 to 0·32]), 21 (50%) in the ervogastat 150 mg group (0·12 [-0·07 to 0·30]), and 14 (45%) in the ervogastat 300 mg group (0·07 [-0·12 to 0·27]). 23 (66%) patients in the ervogastat 150 mg plus clesacostat 5 mg group (difference from placebo 0·27 [90% CI 0·07 to 0·43]) and 19 (63%) of those in the ervogastat 300 mg plus clesacostat 10 mg group (0·25 [0·04 to 0·42]) achieved the composite primary endpoint. Thus, the primary endpoint was not met by any doses of ervogstat alone, but was met by both dose levels of ervogastat plus clesacostat. All experimental groups showed greater effects on MASH resolution without worsening of fibrosis than with placebo alone; improvement in fibrosis by one stage or more without worsening of MASH was not greater in any experimental group compared with placebo. Most adverse events were mild or moderate in severity and did not increase in frequency or severity with increasing dose; however, ervogastat plus clesacostat was associated with a likely undesirable fasting lipid and apolipoprotein profile. The most common adverse event was inadequate control of diabetes (placebo: 4/34 [12%]; ervogastat 25 mg: 6/35 [17%]; ervogastat 75 mg: 5/48 [10%]; ervogastat 150 mg: 3/42 [7%]; ervogastat 300 mg: 2/31 [6%]; ervogastat 150 mg plus clesacostat 5 mg: 2/35 [6%]; ervogastat 300 mg plus clesacostat 10 mg: 2/30 [7%]). There were no fatal events; 19/255 (7%) patients reported 20 serious adverse events (placebo: 1/34 [3%]; ervogastat 25 mg: 1/35 [3%]; ervogastat 75 mg: 5/48 [10%]; ervogastat 150 mg: 1/42 [2%]; ervogastat 300 mg: 4/31 [13%]; ervogastat 150 mg plus clesacostat 5 mg: 5/35 [14%]; ervogastat 300 mg plus clesacostat 10 mg: 2/30 [7%]).

INTERPRETATION:

The combined efficacy, safety, and tolerability data with ervogastat supports continued investigation for its use in MASH. Larger and longer trials are needed to further assess ervogastat and ervogastat plus clesacostat for MASH treatment.

FUNDING:

Pfizer.

01 Feb 2025·CPT-Pharmacometrics & Systems Pharmacology

Exposure–response modeling of liver fat imaging endpoints in non‐alcoholic fatty liver disease populations administered ervogastat alone and co‐administered with clesacostat

Article

Author: Wojciechowski, Jessica ; Hughes, Jim H. ; Vourvahis, Manoli ; Amin, Neeta B.

Abstract:

Non‐alcoholic fatty liver disease and non‐alcoholic steatohepatitis describe a collection of liver conditions characterized by the accumulation of liver fat. Despite biopsy being the reference standard for determining the severity of disease, non‐invasive measures such as magnetic resonance imaging proton density fat fraction (MRI‐PDFF) and FibroScan® controlled attenuation parameter (CAP™) can be used to understand longitudinal changes in steatosis. The aim of this work was to describe the exposure–response relationship of ervogastat with or without clesacostat on steatosis, through population pharmacokinetic/pharmacodynamic (PK/PD) modeling of both liver fat measurements simultaneously. Population pharmacokinetic and exposure–response models using individual predictions of average concentrations were used to describe ervogastat/clesacostat PKPD. Due to both liver fat endpoints being continuous‐bounded outcomes on different scales, a dynamic transform‐both‐sides approach was used to link a common latent factor representing liver fat to each endpoint. Simultaneous modeling of both MRI‐PDFF and CAP™ was successful with both measurements being adequately described by the model. The clinical trial simulation was able to adequately predict the results of a recent Phase 2 study, where subjects given ervogastat/clesacostat 300/10 mg BID for 6 weeks had a LS means and model‐predicted median (95% confidence intervals) percent change from baseline MRI‐PDFF of −45.8% and −45.6% (−61.6% to −31.8%), respectively. Simultaneous modeling of both MRI‐PDFF and CAP™ was successful with both measurements being adequately described. By describing the underlying changes of steatosis with a latent variable, this model may be extended to describe biopsy results from future studies.

News (Medical) associated with Clesacostat

03 Feb 2026

·www.fiercebiotech.com

Pfizer CEO says pipeline pruning is mostly finished after 6 more early-stage culls, $4.4B in impairment charges

After announcing six newly dropped early-stage assets, Pfizer CEO Albert Bourla, Ph.D., told investors that he expects the pharma\'s pipeline pruning to be mostly finished.\n Pfizer has pumped the brakes on six early-stage assets, including three being tested for ulcerative colitis.The Big Pharma has also ceased development of disitamab vedotin, an antibody-drug conjugate (ADC), in bladder cancer, with the company instead set to focus on approved ADC Padcev (enfortumab vedotin) in that setting, Chief Financial Officer David Denton said during Pfizer’s Feb. 3 earnings call (PDF).Overall, the company\'s pipeline adjustments during the fourth quarter resulted in $4.4 billion in impairment charges, Denton added. Disitamab vedotin is still being explored in other HER2-positive cancers, according to Pfizer’s website.Pfizer picked up both Padcev and disitamab vedotin through its $43 billion buyout of Seagen in 2023. The pharma dropped two other Seagen ADCs last November, part of a group of 11 discontinuations at that time.Despite this winnowing of its Seagen haul, Denton said that overall, “the Seagen portfolio is progressing ahead of our expectations.” The three newly dropped phase 1 colitis candidates are CCR6 antagonist PF-07054894, SIK inhibitor PF-07899895 and PF-06414300. Two other assets headed to the scrap heap are PF-07853578, a PNPLA3 modulator that was being studied in metabolic dysfunction-associated steatohepatitis, and anemia candidate PF-07940369. Pfizer has not yet disclosed the modalities of PF-06414300 and PF-07940369, a company spokesperson told Fierce.At the time of publication, Pfizer had not responded to questions from Fierce about the reasons behind the culls or whether they represent a shift away from ulcerative colitis. Pfizer is currently less than a year in to an autoimmune disease collaboration with Flagship Pioneering, part of the duo’s broader multibillion-dollar partnership.Pfizer also shelved a MASH program last quarter, a combo therapy of DGAT2i inhibitor ervogastat and acetyl-CoA carboxylase inhibitor clesacostat.The final of the six newly dropped programs is a phase 1 combo of prifetrastat and atirmociclib in metastatic breast cancer. Both small molecules are still being developed as cancer monotherapies. Asked during Pfizer’s earnings call if more pipeline pruning is expected going forward, CEO Albert Bourla, Ph.D., said the company has “done most of our pruning of our pipeline right now.”“The things that we are continuing right now, at large, are things that we believe they are the ones to invest,” Bourla said.2025 was a year of prioritizing and focusing Pfizer’s portfolio, Chief Scientific Officer Chris Boshoff, M.D., Ph.D., added, which led to “up to $500 million savings in R&D, which is now reinvested in phase three programs.”But that doesn’t mean Pfizer plans on setting its pipeline in stone, Bourla said.“When you speak about realigning, creating synergies, or creating cost savings in R&D that we reinvest, we don\'t mean going forward with this configuration of programs,” the chief exec said. Instead, Pfizer plans to increase its number of programs “by deploying AI, which already happened in 2025 with excellent results.”

Phase 1AcquisitionADCPhase 2

09 Jan 2026

·www.fiercebiotech.com

Madrigal pays $50M for Pfizer MASH drug with eye on Rezdiffra combo potential

The plan for this year is to conduct a drug-to-drug interaction study of ervogastat with Rezdiffra as well as consult with the FDA on the design of a phase 2 combination trial.\n Madrigal has paid Pfizer $50 million for the rights to a DGAT2i inhibitor with the intention of combining the drug with its approved liver disease med Rezdiffra.Madrigal’s thyroid hormone receptor-beta (THR-beta) agonist Rezdiffra became the first-ever drug to be approved by the FDA for metabolic dysfunction-associated steatohepatitis (MASH) back in 2024. The therapy has proven a hit for the company, which is expecting full-year sales for 2025 to top $1 billion.The idea behind acquiring Pfizer’s DGAT2i inhibitor, called ervogastat, is to expand Rezdiffra’s potential. The plan for this year is to conduct a drug-to-drug interaction study of ervogastat and Rezdiffra as well as consult with the FDA on the design of a phase 2 trial for a combination treatment of both drugs.DGAT-2 inhibitors block the final step in triglyceride assembly and storage, resulting in lower hepatic triglycerides, reduced lipotoxic fat and decreased inflammation, Madrigal explained in the Jan. 9 release.“This differentiated mechanism offers the potential for additive clinical benefit when combined with Rezdiffra, a THR-β agonist that increases the cell’s ability to process fat via mitochondrial biogenesis,” the biopharma added.Madrigal also pointed to phase 2 data showing that 72% of patients treated with 150 mg ervogastat achieved at least a 30% reduction in liver fat, while 61% achieved at least a 50% reduction.Ervogastat was an asset in need of a good home. In November, Pfizer announced it was ending work on a MASH combination treatment of ervogastat and an acetyl-CoA carboxylase inhibitor called clesacostat. While Pfizer continued to list ervogastat in its pipeline as a monotherapy, there didn’t appear to be any further trials planned for the drug. In return for the license to ervogastat—along with the rights to two undisclosed early-stage MASH assets—Madrigal has handed over $50 million upfront. While potential milestone payments are also attached to the deal, the companies didn’t share those details.“Our global license agreement for ervogastat aligns with our long-term leadership ambition, and we believe Madrigal is uniquely positioned to advance this promising phase 2 asset and unlock its full clinical and commercial value through a development program focused on combination therapy with Rezdiffra,” Madrigal CEO Bill Sibold said in this morning’s release.Madrigal may have been the first to score an approval for the tricky indication of MASH, but there is plenty of competition on the horizon—including from Novo Nordisk’s GLP-1 Wegovy, which gained an FDA label expansion for the disease last year.“MASH is a complex disease that will require multiple treatment approaches to address the full spectrum of patient needs,” Madrigal’s Chief Medical Officer David Soergel, M.D., said in today’s release.“With Rezdiffra as the anchor and a world-class R&D team, our broadened portfolio now spans several key pathways that will define the future of MASH treatment,” Soergel added. “Along with studies of our oral GLP-1 receptor agonist, we look forward to adding ervogastat to our growing clinical program.\"

Phase 2License out/inClinical ResultDrug ApprovalAcquisition

09 Jan 2026

·firstwordpharma.com

Madrigal scoops Pfizer's shelved MASH drug

Already at the head of the metabolic dysfunction-associated steatohepatitis (MASH) pack, Madrigal Pharmaceuticals is looking to firm up its position with a new deal for a pipeline asset recently cast aside by Pfizer.On Friday, Madrigal said it struck an exclusive global licensing agreement with Pfizer for ervogastat, a Phase II oral DGAT-2 inhibitor that had previously been part of the latter's internal MASH programme and was being developed as a combination with clesacostat, a liver-targeted inhibitor of acetyl-CoA carboxylase (ACC), before being shelved late last year.Madrigal will pay Pfizer $50 million upfront, with additional unspecified milestone payments and royalties tied to future development and sales.Madrigal's Rezdiffra (resmetirom) was the first FDA-approved treatment for non-cirrhotic MASH patients when it was cleared in 2024. The THR-β selective agonist, also approved in Europe, generated $287.3 million in its most recently reported quarter and is tracking toward $1 billion in annual revenues, CEO Bill Sibold has said."With Rezdiffra as the anchor…our broadened portfolio now spans several key pathways that will define the future of MASH treatment," David Soergel, chief medical officer, said in a release Friday. "Along with studies of our oral GLP-1 receptor agonist, we look forward to adding ervogastat to our growing clinical programme."Combo possibilitiesErvogastat targets the final stage of how the liver assembles and stores triglycerides, interrupting the process before toxic fat can accumulate, trigger inflammation and damage liver tissue. Madrigal cited a published Phase II study where 72% of patients treated with a 150-mg dose of ervogastat saw their liver fat drop by at least nearly a third, while 61% achieved reductions of half or more, as measured by MRI-PDFF scans. Patients also showed better liver enzyme levels and reduced liver stiffness on vibration-controlled transient elastography, and all active doses were well tolerated."Because Rezdiffra and ervogastat act on distinct yet complementary pathways that drive liver fat accumulation, this combination has potential to produce additive antisteatotic and antifibrotic efficacy," said Quentin Anstee, lead investigator on the Phase II study.Madrigal plans to conduct a drug-to-drug interaction study with Rezdiffra this year and consult with the FDA on the design of a possible Phase II combination trial.Last July, Madrigal bet up to $2.1 billion for exclusive worldwide rights to a GLP-1 agonist called SYH2086 under an agreement with CSPC Pharmaceutical in a bid to create a best-in-class oral combination therapy for MASH.Despite being first with a marketed treatment for MASH, Madrigal is no longer alone after Novo Nordisk's Wegovy (semaglutide) was granted an accelerated FDA approval — a first for a GLP-1 drug in the disease — last August (see – KOL Views Q&A: Wegovy and Rezdiffra could be friends with mutual benefits in MASH). Eli Lilly has also been trying to capture a piece of the MASH pie with its dual GLP-1/GIP drug tirzepatide.

Phase 2Drug ApprovalLicense out/inClinical ResultAccelerated Approval

100 Deals associated with Clesacostat

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Indication	Highest Phase	Country/Location	Organization	Date
Fibrosis	Phase 2	United States	Pfizer Inc.	15 Jun 2020
Fibrosis	Phase 2	China	Pfizer Inc.	15 Jun 2020
Fibrosis	Phase 2	Japan	Pfizer Inc.	15 Jun 2020
Fibrosis	Phase 2	Bulgaria	Pfizer Inc.	15 Jun 2020
Fibrosis	Phase 2	Canada	Pfizer Inc.	15 Jun 2020
Fibrosis	Phase 2	Hong Kong	Pfizer Inc.	15 Jun 2020
Fibrosis	Phase 2	India	Pfizer Inc.	15 Jun 2020
Fibrosis	Phase 2	Poland	Pfizer Inc.	15 Jun 2020
Fibrosis	Phase 2	Slovakia	Pfizer Inc.	15 Jun 2020
Fibrosis	Phase 2	South Korea	Pfizer Inc.	15 Jun 2020

Clinical Result

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04321031 (MIRNA, CTgov)	Phase 2	Metabolic Dysfunction Associated Steatohepatitis \| Fibrosis	256	Placebo	uxlrkjuggb(zgwqruahbq) = zvdmioovgw vpqhvqazyt (sxbbpcrleg, arkjvoejua - abvijiljom) View more	-	21 Mar 2025
NCT04399538 (CTgov)	Phase 2	Metabolic Dysfunction Associated Steatohepatitis	75	Placebo	wurauemkju(rbgxvwoxgm) = tdhkcznxma uarwsyrvdu (wmyyatayhe, ohvjofuvyw - zsabipvore) View more	-	13 Apr 2023
NCT03776175 (CTgov)	Phase 2	Metabolic dysfunction-associated steatotic liver disease	99	Placebo	qdqwogurhl(mnthqspxjr) = gnkbwiybkh jgkvzmovag (krvnmczxkh, ckekxegogm - bpevakshts) View more	-	23 Sep 2020
NCT03248882 (CTgov)	Phase 2	Metabolic Dysfunction Associated Steatohepatitis	305	Placebo	bepluolrrz(keybtdrykm) = bppogsuxsh iruywmmxov (ejuatkgdad, lhxlrkjunz - xqlsxqmkvv) View more	-	10 Mar 2020
NCT03309202 (CTgov)	Phase 1	Hepatic Insufficiency	24	PF-05221304 (Cohort 1 (Without Hepatic Impairment))	qzlxmiibxh(aomyhdwigz) = xmgzualnan omypvryrhe (yymqdicpzh, 20) View more	-	08 Aug 2019
NCT03309202 (CTgov)	Phase 1	Hepatic Insufficiency	24	PF-05221304 (Cohort 2 (Mild Hepatic Impairment))	qzlxmiibxh(aomyhdwigz) = okcwcnyxri omypvryrhe (yymqdicpzh, 33) View more	-	08 Aug 2019

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