A Phase 3, long-term active treatment extension study of mongersen (GED-0301) in subjects with Crohn's disease (REVOLVE OLE)
1st November 2016 - ongoing
Specialism: Lower GI, Inflammatory Bowel Disease (IBD).
Are you early on in your Crohn’s disease diagnosis or never received biologic treatment?
Are your treatments so far not really working for you?
Would you like to be a part of a trial into a new medication for Crohn’s disease?
To find out if you meet the criteria or to find out any further information please contact research nurses:
Emma Connor: email@example.com 07974259381
Sarah McCorkell: firstname.lastname@example.org 07585984316
Mongersen (GED-0301) is being studied for the treatment of subjects with active Crohn’s disease (CD). Although the etiology of CD has not been completely elucidated, there has been significant advancement in the understanding of the disease pathogenesis. There is evidence that the chronic intestinal inflammation is caused by an excessive immune response to mucosal antigens that is not appropriately controlled by the normal counter-regulatory mechanisms. One of the counter-regulatory mechanisms involves transforming growth factor-beta 1 (TGF-β1). TGF-β1 is a multifunctional factor that has been shown to be involved in regulating growth, differentiation, and function of immune and nonimmune cells. TGF-β1 has been shown to play an important role in the control of immune homeostasis and acts as a potent negative regulator of mucosal inflammation. TGF-β1 knockout mice developed a severe multiple-organ inflammatory disease, in which the lymphocytic infiltration of the affected organs was associated with increased production of tumor necrosis factor-alpha (TNF-α) and interferongamma (IFN-γ). Studies have shown that abrogation of TGF-β1 signaling in T cells alone is sufficient to disrupt T and B cell homeostasis and induce T cell-mediated inflammatory lesions in various organs, including the intestine. It has been widely demonstrated that neutralization of TGF-β1 results in the induction and/or amplification of pathogenic responses responsible for the development of experimental colitis resembling either CD or ulcerative colitis (UC).
GED-0301 is an antisense oligodeoxynucleotide that is complementary to the sequence of the messenger ribonucleic acid (mRNA) transcript of Smad7, and consequently inhibits Smad7 mRNA. GED-0301 is formulated as a gastro-resistant delayed release pH-dependent tablet designed to deliver the active substance in the distal gastrointestinal (GI) tract. This formulation is not intended to achieve systemic absorption, but rather to obtain a local release and therapeutic benefit directly on the intestinal inflammatory lesions. This information supports the potential efficacy of GED-0301 in the treatment of CD.
|Dr Gordon Moran||Dr Moran did his undergraduate medical training at University of Malta Medical School and was awarded an MD in 1999. He completed his basic postgraduate training at St. Luke's Hospital in Malta and gained membership of the Royal College of Physicians of…|
|Dr Sunil Samuel|