Pancreatic Cancer -

October 6, 2015
Pancreatic cancer

Patients with pancreatic cancer often suffer from cachexia, which can have a significant impact on survival and performance status.[1] Dysregulated JAK-STAT activity (resulting from elevated levels of pro-inflammatory cytokines) is believed to play a key role in the development of cachexia, as well as in the growth and proliferation of pancreatic cancer cells and resistance to chemotherapeutic agents.[2-3]

Top-line results from RECAP (Phase II Study of Ruxolitinib Efficacy And Safety In Combination with Capecitabine for Subjects With Recurrent Or Treatment-Refractory Metastatic Pancreatic Cancer), a double-blind, placebo-controlled trial (, showed a hazard ratio for overall survival of 0.47 favoring the ruxolitinib arm in a prospectively defined subgroup of the patients, pre-selected as most likely to benefit from JAK pathway inhibition. The subgroup of interest represented approximately half of the randomized study population.

The U.S. Food and Drug Administration (FDA) has granted orphan status for ruxolitinib for the treatment of pancreatic cancer. Additionally, the Phase III program, which is expected to begin enrollment in the first half of 2014, includes a Special Protocol Assessment (SPA) for a registration trial of patients who failed or were intolerant to first-line therapy and who are part of the subgroup that showed benefit in the RECAP trial. The Phase III program includes a second nearly identical Phase III trial.


  1. Bachmann J, Ketterer K, Marsch C et al. Pancreatic cancer-related cachexia: influence on metabolism and correlation to weight loss and pulmonary function. BMC Cancer. 2009,9:255 [open access].
  2. Marc E. Martignoni M, Kunze P et al. Role of mononuclear cells and inflammatory cytokines in pancreatic cancer-related cachexia. Clin Cancer Res. 2005;11(16):5802-8.
  3. Okitsu K, Kanda T, Imazeki F, et al. Involvement of interleukin-6 and androgen receptor signaling in pancreatic cancer. Genes & Cancer. 2010;1(8):859-67.