Open Clinical Trials

Primary biliary cholangitis (PBC) is an autoimmune liver disease that is treated with Ursodeoxycholic acid. Seladelpar is a PPAR delta agonist that has been shown to be effective in normalizing alk phos in those who fail to respond to Ursodiol. This trial will assess the effectiveness of seladelpar.

Subjects must meet the following criteria to be eligible for study participation:

18 to 75 years old (inclusive)

Male or female with a diagnosis of PBC based on history

UDCA for the 12 months prior to screening (with stable dose for >3 months prior to screening) OR intolerant to UDCA (last dose of UDCA >3 months prior to screening)

ALP >1√óULN and <1.67√óULN

Females of reproductive potential must use at least 1 barrier contraceptive and a second effective birth control method during the study and for at least 90 days after the last dose. Male subjects who are sexually active with female partners of reproductive potential must use barrier contraception, and their female partners must use a second effective birth control method during the study and for at least 90 days after the last dose.

Study Coordinator:
Vyvian Ngo
650-498-9125 
vyviann@stanford.edu

PI: Dr Aparna Goel: goela21@stanford.edu

Metabolic dysfunction-associated steatotic liver disease is the most common liver disease worldwide. Present in approximately 25% of the United States population, these individuals are at risk for progressive liver disease and the development of metabolic dysfunction-associated steatohepatitis (MASH) that can lead to progressive fibrosis and cirrhosis.   This trial is evaluating a novel glucagon-like peptide 1 receptor (GLP-1R) and glucagon receptor (GCGR) agonist, Pemvidutide in the treatment of those with MASH and stage 2-3 fibrosis on liver biopsy.

Inclusion criteria

Metabolic dysfunction-associated steatotic liver disease is the most common liver disease worldwide. Present in approximately 25% of the United States population, these individuals are at risk for progressive liver disease and the development of metabolic dysfunction-associated steatohepatitis (MASH) that can lead to progressive fibrosis and cirrhosis.   This is a Phase 3, randomized, double-blind, placebo-controlled study

evaluating the safety and efficacy of of the FGF-21 analogue efruxifermin in subjects with noncirrhotic NASH/MASH and fibrosis stage 2 or 3 (F2 or F3).  

Inclusion

Males and non-pregnant, non-lactating females between 18–80  years of age,

Previous history or presence of T2D (as determined by medical history or based on screening lab values if previously undiagnosed [i.e., HbA1c ≥ 6.5%]) or 2 out of 4 components of metabolic syndrome (obesity, dyslipidemia, elevated blood pressure, elevated fasting glucose).

Body mass index (BMI) ≥ 25.0 kg/m2. 4

Screening visit: a. FibroScan® liver stiffness measurement (LSM) > 8.5 kPa; b. Enhanced Liver Fibrosis (ELF) score ≥ 9.8; c. Aspartate aminotransfer4. ase (AST) > 35 U/L at Screening;

Estimated glomerular filtration rate (eGFR) ≥ 15 mL/min/1. at Screening; b. Hemoglobin A1c (HbA1c) ≤ 9.5% at Screening.

 Total bilirubin < 1.3 mg/dL at Screening and Pre-baseline and direct bilirubin ≤ 0.5 mg/dL at Screening.

 Platelet count ≥ 100,000/μL at Screening; g. Triglyceride (TG) level ≤ 500 mg/dL at

Cohort 1: Biopsy-proven NASH/MASH. Must have had a liver biopsy obtained ≤ 180 days prior to screening with fibrosis stage 2 or 3 and a non-alcoholic fatty liver disease (NAFLD) activity score (NAS) of ≥ 4 with at least 1 point in each of the following components: 1. Steatosis (scored 0 to 3), 2. Ballooning degeneration (scored 0 to 2), and 3. Lobular inflammation (scored 0 to 3) b. Cohort 2: Biopsy-proven fibrosis stage 3. Subjects with NAS <4 may be enrolled and are not required to meet 1 point in each of the components of NAS.

Study Coordinator:  
Jennifer Smart 
650-721-8517 
jsmart2@stanford.edu

PI: Dr Paul Kwo: pkwo@stanford.edu

This is a Phase 3, randomized, double-blind, placebo-controlled study

evaluating the safety and efficacy of of the FGF-21 analogue Pegozafermin in Subjects with Compensated Cirrhosis due to Metabolic Dysfunction-Associated Steatohepatitis (MASH).

 Subjects must be 18 to 75 years of age inclusive, at the time of signing the ICF.

 Subjects must have at least one metabolic risk factor as listed below:

a. Waist circumference of >94 cm for males, >80 cm for females

b. T2DM (as determined by medical history ≥3 months before Screening); or fasting glucose levels ≥100 mg/dL; or HbA1c ≥5.7%; or treatment for T2DM.

c. Increased fasting triglycerides (≥150 mg/dL) or on lipid lowering treatment

d. Reduced fasting HDL-c (<40 mg/dL for males and <50 mg/dL for females) or on lipid lowering treatment

e. Hypertension or on treatment for hypertension; or ≥130 mmHg systolic blood pressure (BP) or ≥85 mmHg diastolic BP

f. BMI at Screening ≥25.0 (≥23.0 for Asian subjects) and <50.0 kg/m2

Diagnostic criteria for compensated cirrhosis due to MASH. Subject must meet both criteria of compensated cirrhosis and MASH etiology

Evidence of compensated cirrhosis — subject must meet the following two criteria:

i. Current or historical biopsy* with confirmed cirrhosis per current central pathology evaluation

ii. Child-Turcotte-Pugh Class A

Exclusion Criteria

a. ALT or AST ≥250 U/L

b. Alkaline phosphatase >2x upper limit of normal (ULN)

c. Elevation of total bilirubin (>1.3 mg/dL). Subjects with isolated indirect hyperbilirubinemia (normal direct bilirubin) secondary to medically documented Gilbert’s syndrome may be enrolled

d. Triglycerides >1000 mg/dL

e. INR >1.30 unless due to anti-coagulant therapy. Subjects on anti-coagulant therapy may require their treatment withheld according to local guidelines prior to liver biopsy.

f. eGFR <50 mL/min/1.73 m2 as estimated by chronic kidney disease-epidemiology (CKD-EPI) creatinine equation (Inker, 2021)

g. Platelet count <100,000/μL

h. MELD Score >12

i. Albumin ≤3.5 g/dL

Study Coordinator:  
Jennifer Smart 
650-721-8517 
jsmart2@stanford.edu

PI: Dr Paul Kwo: pkwo@stanford.edu

The purpose of this protocol is to evaluate the efficacy and safety of tulisokibart in participants with moderately to severely active Crohn's disease. Study 1's primary hypotheses are that at least 1 tulisokibart dose level is superior to Placebo in the proportion of participants achieving clinical remission per Crohn's Disease Activity Index score (<150, US/FDA)   and in the proportion of participants achieving endoscopic response at Week 52 (US/FDA), and that at least 1 tulisokibart dose level is superior to Placebo in the proportion of participants achieving clinical remission per Crohn's Disease Activity Index score (<150) or per stool frequency and abdominal pain score and in the proportion of participants achieving endoscopic response at Week 12 (US/FDA). Study 2's primary hypothesis is that at least one tulisokibart dose level is superior to Placebo in the proportion of participants achieving clinical remission per Crohn's Disease Activity Index score (<150) and in the proportion of participants achieving endoscopic response at Week 12 (US/FDA and EU/EMA).

1. Has moderately to severely active CD as defined by CDAI 220 – 450 at Baseline.
2. Has SES-CD score (excluding the presence of narrowing component) ≥6 if ileocolonic -or- colonic disease; or ≥4 if isolated ileal disease only, as confirmed by a central reader.
3. Average daily very soft or liquid SF ≥4 and/or average daily APS ≥2 at Baseline.
4. Demonstrated inadequate response, loss of response, or intolerance to one or more of the following categories of drugs: oral locally acting steroids, systemic steroids, immunomodulators, biologic and/or small molecule advanced therapies.
5. Inadequate response is defined to steroids, immunomodulators, and biologic therapies.

Study Coordinator:
Briana Cavalla
650-724-1084
Cavallab@stanford.edu


PI: Dr Sarah Streett: sstreett@stanford.edu