CNI-1493 for Treatment of Moderate to Severe Crohn's Disease

Crohn Disease Clinical Trial

— CD02  

Official title:

A Randomized, Double-Blind, Placebo-controlled Study of CNI-1493 for Treatment of Moderate to Severe Crohn's Disease

Clinical Trial Details — Status: Terminated

Administrative data

• NCT number: NCT00038766
• Other study ID #: CNI-1493 CD-02
• Status: Terminated
• Phase: Phase 2
• First received: June 5, 2002
• Last updated: August 22, 2012
• Start date: June 2002
• Est. completion date: June 2003

Study information

• Verified date: August 2012
• Source: Ferring Pharmaceuticals
• Contact: n/a
• Is FDA regulated: No
• Health authority: United States: Food and Drug Administration
• Study type: Interventional

Clinical Trial Summary

The purpose of this study is to determine whether CNI-1493 is safe and effective in the treatment of moderate to severe Crohn's Disease.

Description:

Crohn's disease (CD) is a chronic inflammatory disease involving the upper and lower gastrointestinal tract and characterized by abdominal pain, weight loss, gastrointestinal bleeding and formation of fistulas between loops of bowel and from the bowel to the skin or other organs. Current therapy for active Crohn's disease consists of symptomatic treatment, nutritional therapy, salicylates and immunosuppressants or surgical management.

Tumor necrosis factor a (TNF-a) plays a central role in the initiation and amplification of the granulomatous inflammatory reaction seen in CD (van Deventer, 1997). Increased TNF-a is present in gut mucosa as well as in stool of patients with active CD (Braegger et al, 1992). CNI-1493 is a synthetic guanylhydrazone compound that is an inhibitor of TNF-a synthesis. A monoclonal antibody to TNF, infliximab, is now approved for treatment of CD, but not all patients respond and many who do respond eventually become refractory to this treatment as well.

CNI-1493 is a synthetic compound which blocks the production of several inflammatory cytokines, including TNF. Because it blocks production of multiple inflammatory mediators, it may be more active than products targeted to a specific cytokine. In addition, as it is not a biologic, it should not cause hypersensitivity reactions or induce formation of antibodies.

The purpose of this trial is to determine if CNI-1493 is safe and effective in treating patients with moderate to severe Crohn's Disease in a placebo controlled setting.

Recruitment information / eligibility

• Status: Terminated
• Enrollment: 33
• Est. completion date: June 2003
• Est. primary completion date: June 2003
• Accepts healthy volunteers: No
• Gender: Both
• Age group: 18 Years and older

Eligibility

Inclusion Criteria

• Baseline Crohn's Disease Activity Index (CDAI) 250-400, inclusive

• Crohn's disease of at least 3 months duration, with colitis, ileitis, or ileocolitis, confirmed by radiography and/or endoscopy

• Patients receiving medications for CD must be on stable doses entering the study

• Any CD medication which has been discontinued must have been discontinued at least 4 weeks prior to screening, with the exception of infliximab, which must have been discontinued at least 8 weeks prior to screening

Exclusion Criteria

• Patients with any ostomy or extensive bowel resection

• Current evidence of bowel obstruction or history within the preceding six months as confirmed by radiography, endoscopy, or surgery

• Patients with stool examination positive for enteric pathogens, pathogenic ova or parasites, or Clostridium difficile toxin

• Treatment with any other experimental therapeutics within the last 4 weeks before enrollment

Study Design

Allocation: Randomized, Endpoint Classification: Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor), Primary Purpose: Treatment

Related Conditions & MeSH terms

• Crohn Disease

Intervention

Drug:
• semapimod
semapipmod 60 mg IV x 5 days
• semapimod
IV 30 mg x 5 days
• placebo
placebo IV

Locations

Country	Name	City	State
United States	Atlanta Gastroenterology Associates	Atlanta	Georgia
United States	Charlotte Gastroenterology and Hepatology, PLLC	Charlotte	North Carolina
United States	Northwestern University	Chicago	Illinois
United States	University of Chicago	Chicago	Illinois
United States	University of Florida	Gainesville	Florida
United States	Long Island Clinical Research Associates	Great Neck	New York
United States	Regional Gastroenterology Associates of Lancaster, Ltd.	Lancaster	Pennsylvania
United States	Mount Sinai School of Medicine	New York	New York
United States	Digestive and Liver Disease Specialists	Norfolk	Virginia
United States	Oklahoma Foundation for Digestive Research	Oklahoma City	Oklahoma
United States	Wake Research Associates	Raleigh	North Carolina
United States	Institute of Healthcare Assessment	San Diego	California
United States	Washington University School of Medicine	St. Louis	Missouri

Sponsors (1)

Lead Sponsor	Collaborator
Ferring Pharmaceuticals

Country where clinical trial is conducted

United States, 

References & Publications (1)

Hommes D, van den Blink B, Plasse T, Bartelsman J, Xu C, Macpherson B, Tytgat G, Peppelenbosch M, Van Deventer S. Inhibition of stress-activated MAP kinases induces clinical improvement in moderate to severe Crohn's disease. Gastroenterology. 2002 Jan;122(1):7-14. — View Citation

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Change in CDAI		Day 29	No
Secondary	Change in IBDQ		Day 29	No