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Christopher Bowlus, M.D.

· Chief, Division of Gastroenterology and Hepatology, Lena Valente ProfessorVerified

University of California, Davis · Gastroenterology, Hepatology and Nutrition

Active 1987–2026

h-index66
Citations14.8k
Papers400123 last 5y
Funding
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About

Christopher Lawson Bowlus, M.D., is the Chief of the Division of Gastroenterology and Hepatology at UC Davis Health. He specializes in the care of patients with liver disease and has expertise in managing autoimmune liver diseases, including primary biliary cholangitis, primary sclerosing cholangitis, and autoimmune hepatitis. Dr. Bowlus is interested in elucidating the underlying genetic and immunologic causes of autoimmune liver diseases and using this information to develop more effective treatments for these conditions. His research and academic interests focus on understanding the pathogenesis of autoimmune liver diseases and improving therapeutic strategies.

Research topics

  • Medicine
  • Internal medicine
  • Gastroenterology
  • General surgery
  • Immunology
  • Oncology
  • Bioinformatics
  • Intensive care medicine
  • Emergency medicine
  • Environmental health
  • Biology
  • Pathology

Selected publications

  • Seladelpar in patients with primary biliary cholangitis and compensated cirrhosis: Efficacy and safety from RESPONSE and ASSURE studies

    Hepatology Communications · 2026-04-13

    articleOpen access

    BACKGROUND: Treatment options are limited for patients with primary biliary cholangitis (PBC) and cirrhosis. Seladelpar, a first-in-class delpar (selective PPAR-δ agonist), had generally similar efficacy and safety among patients with versus without compensated cirrhosis in the phase 3 RESPONSE study. Here we provide additional data on seladelpar in patients with compensated cirrhosis from the phase 3 program. METHODS: In RESPONSE, patients with PBC and an inadequate response or intolerance to UDCA were randomized 2:1 to seladelpar 10 mg or placebo for 1 year. Upon completion, patients rolled over into the open-label (seladelpar 10 mg) phase 3 ASSURE study, which also enrolled patients from earlier seladelpar legacy PBC studies. Here, we assessed the composite endpoint [alkaline phosphatase (ALP) <1.67×upper limit of normal (ULN), ALP decrease ≥15%, and total bilirubin ≤ULN], other laboratory changes, and safety in all patients with cirrhosis from RESPONSE and an interim analysis of the ongoing ASSURE study through January 2024. RESULTS: Twenty-seven patients with compensated cirrhosis enrolled in RESPONSE (18 seladelpar, 9 placebo). At month 12, 38.9% and 22.2% of patients in the seladelpar and placebo groups, respectively, met the composite endpoint; mean percent change from baseline in ALP was -37.1% and -10.1%, respectively. Upon rollover to ASSURE (13 seladelpar, 6 placebo), ALP declines were maintained for up to 18 months. An additional 35 patients with compensated cirrhosis in ASSURE from legacy studies had similar reductions in ALP with up to 2 years of treatment. Bilirubin remained overall stable. No treatment-related serious adverse events occurred. Variceal bleeding and/or ascites developed in 3 patients after ≥9 months. CONCLUSIONS: Seladelpar decreased markers of cholestasis and was overall safe and well-tolerated in patients with PBC and compensated cirrhosis.

  • 138 - LONG-TERM TREATMENT WITH ELAFIBRANOR LEADS TO BIOCHEMICAL AND SYMPTOMATIC IMPROVEMENTS FOR AT LEAST 3 YEARS IN PATIENTS WITH PRIMARY BILIARY CHOLANGITIS

    Gastroenterología y Hepatología · 2026-02-01

    article
  • 143 - TREATMENT WITH ELAFIBRANOR LEADS TO STABILIZATION OF PRO-C3, A MARKER OF FIBROSIS, IN PATIENTS WITH PRIMARY BILIARY CHOLANGITIS

    Gastroenterología y Hepatología · 2026-02-01

    article
  • 146 - REDUCTION IN ITCH-ASSOCIATED DISABILITY AND PRURITUS DISTRIBUTION IN PATIENTS WITH PRIMARY BILIARY CHOLANGITIS TREATED WITH SELADELPAR IN THE RESPONSE TRIAL

    Gastroenterología y Hepatología · 2026-02-01

    article
  • Cilofexor in non-cirrhotic primary sclerosing cholangitis (PRIMIS): a randomised, double-blind, multicentre, placebo-controlled, phase 3 trial

    Institutional Repositories DataBase (IRDB) · 2026-01-01

    articleSenior author

    BACKGROUND: There is currently no pharmacological therapy proven to alter the natural course of primary sclerosing cholangitis (PSC). The PRIMIS trial evaluated the efficacy and harms of the farnesoid X-activated receptor agonist cilofexor in participants with non-cirrhotic PSC. METHODS: In this phase 3, double-blind, placebo-controlled, multicentre trial (205 sites across 16 countries), adults aged 18-75 years with non-cirrhotic (F0-F3 [Ludwig classification]) large-duct PSC were randomly assigned (2:1) via an interactive web response system to receive cilofexor 100 mg or placebo (identical in appearance) orally once daily for 96 weeks. Randomisation was stratified by ursodeoxycholic acid use (yes or no) and the presence of bridging fibrosis (F3 vs F0-F2), with a block size of six within each stratum. Participants, personnel directly involved in the conduct of the study, and outcome assessors were masked to treatment assignment. The primary endpoint was the proportion of participants with histological progression of liver fibrosis (a stage increase of one or more [Ludwig classification]) at week 96. After study termination, the primary endpoint analysis set was amended to include all participants in the harms analysis set (all who received at least one dose of the study drug) who had biopsy data at baseline and week 96. This trial is complete (ClincalTrials.gov, NCT03890120). FINDINGS: Between June 13, 2019, and July 22, 2021, 419 participants were randomly assigned, and 416 were included in the full and harms analysis sets (cilofexor: n=277; placebo: n=139); 257 (62%) men and 159 (38%) women. The study was terminated early on Sept 26, 2022, after a planned interim futility analysis after 160 patients had reached 96 weeks of follow-up indicated a 6·8% probability of detecting a significant difference between cilofexor over placebo (futility boundary ≤10%). In the final analysis of the primary endpoint, for which 133 patients in the cilofexor group and 64 in the placebo group had liver biopsy results available, fibrosis progression occurred in 41 (31%) participants in the cilofexor group and 21 (33%) in the placebo group at week 96 (treatment difference -1·4% [95% CI -15·2 to 12·3]; p=0·42). The most common adverse events were pruritus (cilofexor: 136 [49%] of 277 patients; placebo: 50 [36%] of 139 patients; grade 3 or higher in 11 [4%] patients in the cilofexor group and one [1%] patient in the placebo group), COVID-19 (cilofexor: 65 [23%]; placebo: 26 [19%]), and upper abdominal pain (cilofexor: 40 [14%]; placebo 20 [14%]). The proportion of serious adverse events was similar between groups (cilofexor: 53 [19%]; placebo: 26 [19%]). There were no treatment-related deaths. INTERPRETATION: Cilofexor did not significantly reduce the rate of fibrosis progression (vs placebo) in participants with non-cirrhotic PSC. A greater percentage of cilofexor-treated participants had pruritus than placebo-treated participants; this study provides valuable harms data for cilofexor and other drugs in its class. FUNDING: Gilead Sciences.

  • Impact of Disease‐Specific Treatment and Non‐Selective Beta Blockers on Risk of <scp>PVT</scp> in Cirrhotic Patients With <scp>HCV</scp> or <scp>PBC</scp>

    Liver International · 2026-04-03 · 1 citations

    articleOpen access

    BACKGROUND: Portal vein thrombosis (PVT) is a common sequela of cirrhosis. Despite regression of fibrosis/cirrhosis observed among some patients after disease-specific treatment, few studies have considered the role of treatment and response on risk of PVT among patients with cirrhosis across different liver disease states. We considered aetiological treatment and response as well as whether non-selective beta-blockers (NSBBs), statins, and anticoagulants were associated with risk of PVT. METHODS: We used data for patients with cirrhosis (compensated or decompensated) from two large, US-based multisite cohort studies. Patients with hepatitis C (HCV) were drawn from the Chronic Hepatitis Cohort Study. Patients with primary biliary cholangitis (PBC) were drawn from the Fibrotic Liver Disease Consortium. Risk for PVT was assessed using a discrete survival model that includes both fixed covariates and time-dependent variables. RESULTS: Among 6659 HCV patients, 274 developed PVT across ~13 years of follow-up. Significant risk factors included time-varying decompensated cirrhosis (adjusted hazard ratio [aHR] 27.41, 95% confidence interval [CI] 15.89-47.30), male sex (aHR 1.48, 95% CI 1.12-1.94), and use of NSBBs (aHR 2.07, 95% CI 1.61-2.67). Among 786 PBC patients, 67 developed PVT across ~8 years of follow-up. Use of NSBBs was the only significant PVT risk factor in these patients (aHR 2.56, 95% CI 1.52-4.31). Neither sustained virological response [SVR] after antiviral treatment (HCV patients) nor response to ursodeoxycholic acid [UDCA] treatment (PBC patients) was associated with risk of PVT. CONCLUSIONS: In two large well-characterized samples of cirrhotic patients with HCV or PBC, disease-specific treatments were not associated with PVT risk. NSBB treatment was independently associated with > 2 times the risk of PVT in both samples, regardless of compensated or decompensated status.

  • FP7 Bexotegrast improves markers and symptoms of cholestasis and stabilizes markers of liver fibrosis in participants with primary sclerosing cholangitis

    2025-06-01

    article
  • O8 Linerixibat significantly improves cholestatic pruritus in primary biliary cholangitis (PBC): results of the pivotal phase 3 GLISTEN trial

    2025-10-01 · 1 citations

    article

    <h3>Introduction</h3> Cholestatic pruritus is common, debilitating and undertreated in patients with PBC. Here, we describe the results of GLISTEN (NCT04950127), a Phase 3 study investigating efficacy and safety of linerixibat (ileal bile acid transporter inhibitor) for pruritus in PBC. <h3>Methods</h3> In this double-blind, randomised, placebo-controlled study, patients with PBC and moderate-to-severe pruritus received oral linerixibat 40 mg or placebo twice daily. Pruritus severity and pruritus-related sleep interference were assessed using a 0–10 numerical rating scale. Primary endpoint was change from baseline in worst itch over 24 weeks. Secondary endpoints included: at Week 2, change in worst itch; over 24 weeks, change in sleep interference; at Week 24, proportion of responders (≥ 2-, ≥ 3-, ≥ 4-point reduction in worst itch) and analysis of responses to 2 patient global impression items (itch severity; change). Safety endpoints included adverse event (AE) reporting. <h3>Results</h3> 238 patients were randomised (95% female); itch severity was mean (standard deviation [SD]) 7.34 (1.54), 52% had alkaline phosphatase &lt;1.67 times upper limit of normal; 47% were receiving stable pruritus therapy. Pruritus improvement over 24 weeks was significantly greater with linerixibat than placebo: least-squares (LS) mean change -2.86 versus -2.15, adjusted mean difference -0.72; p=0.001. At Week 24, observed mean (SD) difference from baseline in pruritus was -3.66 (2.50) with linerixibat and -2.82 (2.32) with placebo. Linerixibat effect was superior to placebo at Week 2: LS mean change -1.78 versus -1.07, adjusted mean difference -0.71; p&lt;0.001. Linerixibat significantly improved pruritus-related sleep interference over 24 weeks versus placebo: LS mean change 2.77 versus -2.24, adjusted mean difference -0.53; p=0.024. At Week 24, more patients on linerixibat than placebo achieved a ≥2-point (68% vs 64%), ≥3-point (56% vs 43%) or ≥4-point (41% vs 29%) reduction in pruritus; a higher proportion of linerixibat than placebo-treated patients reported their pruritus was very much improved (55% vs 37%) or absent (21% vs 9%). AEs reported more frequently with linerixibat than placebo were predominantly gastrointestinal (GI), including diarrhoea (61% vs 18%) and abdominal pain (18% vs 3%); 4% of patients in the linerixibat group discontinued treatment due to diarrhoea. <h3>Summary/Conclusion</h3> In patients with PBC and moderate-to-severe pruritus, linerixibat significantly improved pruritus and pruritus-related sleep interference versus placebo. While GI AEs were more common with linerixibat than placebo, they rarely led to treatment discontinuation. <h3>Funding</h3> GSK [212620/NCT04950127]. Previously presented at EASL 2025 (presentation GS-011) [on behalf of the GLISTEN study group]

  • Nebokitug, an Anti-chemokine (C-C Motif) Ligand 24 Monoclonal Antibody, in Patients With Primary Sclerosing Cholangitis: A Phase 2 Study

    The American Journal of Gastroenterology · 2025-11-19 · 1 citations

    articleOpen access1st authorCorresponding

    INTRODUCTION: Nebokitug (CM-101) is an antichemokine (C-C motif) ligand 24 monoclonal antibody with anti-inflammatory and antifibrotic properties. This phase 2 study evaluated the safety, tolerability, and biological activity of nebokitug in patients with primary sclerosing cholangitis (PSC). METHODS: SPRING was a randomized, double-blind (DB), placebo-controlled phase 2 study in which patients with large duct PSC were randomized to receive IV nebokitug 10 mg/kg, 20 mg/kg, or placebo every 3 weeks for 15 weeks. The primary end point was safety and tolerability. Secondary end points included change from baseline to week 15 in liver blood tests, enhanced liver fibrosis (ELF) score, and liver stiffness measurements (LSM). Biological activity was explored in a prespecified subgroup with moderate/advanced fibrosis. Eligible patients who completed the 15-week DB period entered the open-label extension study to receive nebokitug for a total of 48 weeks. RESULTS: A total of 76 patients were enrolled and received at least 1 dose of nebokitug (n = 56) or placebo (n = 20). Frequency and severity of treatment-emergent adverse events were similar between the groups. No significant changes in liver tests, ELF scores, and LSM from baseline to week 15 were observed in the total treatment population. However, in the prespecified subgroup of patients with moderate/advanced fibrosis (n = 35), patients treated with nebokitug showed a significant reduction in LSM. Of the 54 patients eligible to participate, 50 enrolled in the OLE. Nebokitug continued to be well tolerated, and no new safety signal was observed. DISCUSSION: Nebokitug was well tolerated up to 48 weeks of treatment and demonstrated numerical biomarker improvements in patients with PSC, particularly in those with moderate/advanced fibrosis.

  • Long-term efficacy and safety of open-label seladelpar treatment in patients with primary biliary cholangitis: pooled interim results for up to 3 years from the ASSURE study

    Zeitschrift für Gastroenterologie · 2025-09-01

    article

Frequent coauthors

  • Gideon M. Hirschfield

    University of Toronto

    112 shared
  • Cynthia Levy

    102 shared
  • Pietro Invernizzi

    University of Milano-Bicocca

    69 shared
  • Palak Trivedi

    NIHR Birmingham Biomedical Research Centre

    63 shared
  • Marlyn J. Mayo

    Health Net

    63 shared
  • Kris V. Kowdley

    63 shared
  • M. Eric Gershwin

    59 shared
  • Michael Trauner

    Medical University of Vienna

    54 shared

Labs

  • Gastroenterology and Hepatology, UC Davis HealthPI

Awards & honors

  • Internal Medicine Faculty Research Award, 2020
  • PSC Partners Seeking a Cure Golden Liver Award, 2016
  • PSC Partners Seeking a Cure Visionary Award, 2014
  • Walter Trudeau Excellence in Teaching Award, 2013
  • PSC Partners Seeking a Cure Partner of the Year, 2011
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