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Vercirnon (also known as Traficet-EN, or CCX282) targets the chemokine receptor known as CCR9. Vercirnon is a our Phase III-ready drug candidate for the treatment of patients with moderate-to-severe Crohn's disease, a chronic inflammatory condition of the gastrointestinal tract and one of two forms of inflammatory bowel disease (IBD). Inflammatory bowel disease refers to two diseases, Crohn's disease and ulcerative colitis, both characterized by inflammation of the gastrointestinal tract.

Vercirnon is intended to control the inflammatory response underlying IBD by targeting the chemokine receptor known as CCR9. In adults, CCR9 is found primarily on a population of T cells, a subset of the body's inflammatory cells that migrate selectively to the digestive tract. It is believed that when CCR9's ligand, CCL25 (also known as TECK), is over-expressed, the migration of T cells to the small and large intestine causes persistent inflammation that may result in Crohn's disease or ulcerative colitis, the two forms of IBD. Vercirnon is designed to prevent the migration of inflammatory cells to the digestive tract by blocking the function of CCR9. By interrupting CCR9 signaling, we believe vercirnon may hasten the elimination of inflammatory T cells from the intestines, thus potentially speeding recovery by reducing the longevity of flare-ups associated with IBD.

We believe this mechanism of action would allow vercirnon, if approved, to be a highly effective treatment with significantly fewer side effects than currently available immunosuppressive therapies, including TNF-a inhibitors, providing physicians with a new and attractive option for the treatment of patients with moderate-to-severe Crohn's disease.

We have completed nine clinical trials with vercirnon in a total of 785 subjects, including five Phase I clinical trials in a total of 151 subjects, one Thorough QT study in 57 subjects demonstrating cardiovascular safety, two Phase II clinical trials in 510 patients with Crohn's disease and one Phase II clinical trial in 67 patients with celiac disease. The largest of these Phase II clinical trials, PROTECT-1, was conducted in 436 patients with moderate-to-severe Crohn's disease. Results from this clinical trial indicated that vercirnon was effective in inducing a clinical response over a 12-week treatment period in these patients. Furthermore, the results indicated that vercirnon was also effective in maintaining clinical remission over a 36-week treatment period. Vercirnon was safe and well tolerated in all clinical trials completed to date.

In 2006, we initiated PROTECT-1, a multinational, multi-center Phase II clinical trial to further assess the safety and efficacy of vercirnon for the induction of clinical response or remission in patients with moderate-to-severe Crohn's disease. Following the completion of a 12-week induction phase during which all subjects received either a placebo or one of three doses of vercirnon and a four-week open label active treatment phase during which all subjects received vercirnon, the study included a separate 36-week phase to evaluate vercirnon's utility as maintenance therapy for the response or remission in patients with Crohn's disease. This was accomplished by re-randomizing all subjects with a 70-point-or-greater drop in CDAI scores at the end of the four-week active treatment period to either vercirnon or placebo.

We completed the PROTECT-1 trial. Vercirnon demonstrated evidence of clinical efficacy in the reduction of disease severity, as defined by a decrease from baseline in the Crohn's Disease Activity Index (CDAI) score of at least 70 points over the course of 12 weeks; the more stringent criterion of at least a 100 point decrease in the CDAI score was also met by week 12. In addition, vercirnon was safe and well-tolerated.

Data from the maintenance period of the PROTECT-1 clinical trial showed that more patients receiving vercirnon were in clinical remission by the end of 36 weeks compared to placebo.

In addition, we completed a Thorough QT study in healthy volunteers which showed that there was no deleterious effect on QT/QTc interval with vercirnon at either therapeutic or supratherapeutic doses.

Vercirnon Advantages
We believe that vercirnon may provide the following advantages over existing therapeutic approaches for the treatment of patients with Crohn's disease:

  • Oral administration as a more convenient option relative to injectable or infusible therapeutics such as TNF-α inhibitors as well as certain steroids and immunosuppressants. Patient compliance is particularly important in controlling chronic conditions such as Crohn's disease.

  • Lower manufacturing costs, relative to TNF-α inhibitors, as a small molecule.

CCX507- Next Generation CCR9 Inhibitor for IBD
Building on our expertise in the area of CCR9 antagonists and IBD, we started a de novo discovery program under which we have designed a series of novel molecules that we believe represent the next generation of CCR9 inhibitors. This followed the expiration of our target exclusivity obligations with respect to CCR9 under our collaboration agreement with GSK. The development candidate from this de novo series, CCX507, is selective for CCR9 relative to all other chemokine receptors, orally bioavailable, and has an excellent preclinical safety profile. Preclinical data has demonstrated that CCX507, in combination with an anti-α4β7 (α4β7) blocking antibody, markedly reduced the severity of colitis more effectively in vivo than monotherapy treatment with either CCX507 or an anti-α4β7 blocking antibody alone. Molecules such as CCX507 have been designed to interact with the CCR9 receptor in a unique way that produces molecules with greater potency towards CCR9 than other compounds reported to date. CCX507 is currently in/has completed a Phase I clinical trial whose results showed that CCX507 is safe and well tolerated in healthy volunteers at all doses tested, and effectively blocked CCR9 on circulating leukocytes. We plan to move the compound forward to Phase II clinical trials, potentially in conjunction with a strategic partner.

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