News

TLR9 agonist active against ulcerative colitis in small study


 

AT DDW 2013

ORLANDO – An investigational immunomodulator prosaically named DIMS 0150 was associated with sustained remissions in some patients with ulcerative colitis, reported investigators at the annual Digestive Disease Week.

Among patients with ulcerative colitis (UC) randomized to receive a single rectally delivered dose of DIMS 0150 or placebo, 5 of 16 patients available for 3-month follow-up had a sustained clinical response, compared with none of the eight control patients who received a placebo enema, said Dr. Thomas Knittel from InDex Pharmaceuticals in Stockholm.

The drug contains a single-stranded oligonucleotide that acts as a Toll-like receptor 9 (TLR9) agonist by activating TLR9 when the drug is administered to mucosal surfaces. TLR9 (also called CD289) encodes a protein involved in innate immunity and pathogen recognition and in mediation of anti-inflammatory cytokines, primarily interleukin 10 and interferon-alpha.

In animal studies, activation of TLR9 has been shown to promote healing of UC.

The investigators conducted a randomized, double-blind, placebo-controlled trial of the agent in patients with UC refractory to steroids. A total of 34 patients were randomized to receive on a 2:1 basis (22:12) either a single 30-mg dose of DIMS 0150 delivered via enema, or a placebo enema consisting of only water.

The patients had Disease Activity Index (DAI) scores of 6-11 pts were taking at least 5 mg steroids/day and were judged as either steroid dependent or steroid resistant.

At the end of the first follow-up week, 7 of 17 patients on DIMS 0150 had a clinical response (decrease in DAI score of at least 3 points from baseline), compared with 1 of 11 patients on placebo. By week 4, two additional patients on the TLR9 agonist had achieved a clinical response (9 of 17), as did three additional patients on placebo (4 of 11).

By week 12, 5 of 16 patients who had received DIMS 0150 and completed 12 weeks of therapy still had a clinical response, in contrast to none of the eight patients on placebo who completed 12 weeks of follow-up. However, neither the 4-week nor 12-week follow-up differences in sustained response between the active drug and placebo groups were significant.

Two of 17 patients on DIMS 0150 had a clinical remission (total DAI score of 2 points or less, with no individual subscore higher than 1) at week 1, 3 of 17 were in remission at week 4, and 6 of 16 were in remission at 12 weeks. In contrast, none of the control patients had remissions at either week 1 or week 4, but two of eight controls were in remission at week 12.

The authors also looked at histologic remission (improvement to a score of 0) at all three time points and found that at week 4, 6 of 17 patients on the TLR9 agonist had a remission, vs. 0 of 11 on placebo, a difference that teetered on the edge of statistical significance (P = .055).

Dr. Knittel did not present safety data, but said that in previous studies, the drug at the 30-mg dose has been shown to be safe and that patients tolerated it well.

In response to a question following his presentation, Dr. Knittel noted that the investigators had not measured cytokine levels to determine whether the drug was having its intended effect, but instead relied on clinical findings to determine efficacy.

The phase II study Dr. Knittel presented confirms clinical data obtained in earlier studies of this agent, and "indicates that a single dose of a TLR9 agonist can be effective, and efficacy was observed with respect to clinical response, clinical remission, and histological healing," he said.

But a gastroenterologist who was not involved in the study says that it was lacking data in several key areas, because the investigators did not measure baseline or post-treatment levels of anti-inflammatory cytokines or C-reactive protein and did not perform endoscopies to assess colonic mucosa.

"In ulcerative colitis, that’s where the rubber hits the road: whether the mucosa gets better," said Dr. Maria T. Abreu, chief of gastroenterology and professor of medicine at the University of Miami.

"I don’t expect it to completely resolve, because even in studies of anti-TNF [tumor necrosis factor–alpha], which we believe to be the most potent therapy we have now for mucosal healing, the numbers of patients that actually have the mucosa heal completely in ulcerative colitis is low – only about a quarter of patients have that happen. ... But these investigators didn’t report any change in the endoscopy," Dr. Abreu said.

The study was funded by InDex Pharmaceuticals. Dr. Knittel is chief medical officer and consultant for the company, and two of his coauthors are employees.

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