Pharmabiz
 

New phase 2 results show glasdegib improved overall survival in AML & high-risk MDS

New YorkMonday, December 5, 2016, 16:00 Hrs  [IST]

Pfizer Inc. announced new data from a randomized phase 2 study of glasdegib (PF-04449913), an oral, smoothened (SMO) inhibitor, showing the addition of glasdegib to low-dose cytarabine (LDAC) significantly increased overall survival (OS) when compared to LDAC alone in patients with acute myeloid leukemia (AML) or high-risk myelodysplastic syndrome (MDS) who were ineligible for intensive chemotherapy (HR: 0.501, 80% CI: 0.384, 0.654, one-sided log rank p-value 0.0003). Glasdegib is the first SMO inhibitor to show clinical benefit in this patient population. These data were presented at the 58th American Society of Hematology (ASH) Annual Meeting and Exposition in San Diego, CA.

Glasdegib is an investigational oral therapy that inhibits the SMO receptor, thereby disrupting the hedgehog (Hh) pathway. The results presented are from a phase 2, multicenter, randomized study that included 132 patients with previously untreated AML or high-risk MDS who were ineligible for intensive chemotherapy. Patients were treated with either LDAC 20mg subcutaneously twice daily for ten days plus oral glasdegib 100 mg daily or LDAC alone. The primary endpoint of this study was OS.

“The hedgehog pathway is a compelling target in cancer research because of the ability to target and disrupt the root of the cancer, that is the cancer-originating cell,” said Jorge Cortes, University of Texas, MD Anderson Cancer Center. “As the first smoothened inhibitor to demonstrate clinical benefit in patients with AML and high-risk MDS who were ineligible for intensive chemotherapy, these results with glasdegib provide hope that interfering with this pathway may lead to potential new treatment options for blood cancers that may improve patient outcomes.”

The results presented show that at the time of data cut-off, median OS for patients taking glasdegib plus LDAC (n=88) was 8.8 months (80% CI: 6.9, 9.9) compared to 4.9 months (80% CI: 3.5, 6.0) for patients taking LDAC only (n=44) (HR: 0.501, 80% CI: 0.384, 0.654, one-sided log rank p-value 0.0003). Low blood counts and gastrointestinal toxicities occurred more frequently among patients treated with glasdegib plus LDAC than those treated with LDAC alone. Blood infections were less among patients treated with glasdegib plus LDAC (3.6 %) compared to LDAC alone (12.2%). Patients in the glasdegib plus LDAC group experienced increased distortion of taste (23.8%), muscle spasms (20.2%) and thinning or loss of hair (10.2%). Serious AEs of febrile neutropenia were also more frequent in patients taking glasdegib plus LDAC (36.9%) compared to LDAC alone (26.8%). The most common cause of death in both arms was disease progression.

“Acute myeloid leukemia is a rapidly progressing blood cancer for which new treatment options are needed,” said Mace Rothenberg, MD, chief development officer, Oncology, Pfizer Global Product Development. “Pfizer is excited about the promising data seen in AML patients treated with glasdegib and is working to explore further opportunities to evaluate glasdegib in the treatment of this disease.”

Glasdegib is an investigational oral therapy that inhibits the SMO receptor, thereby disrupting the hedgehog (Hh) pathway. SMO inhibition of Hh signaling impacts tumor biology by disrupting the regulation of cancer stem cell (CSC) survival. This may inhibit development of drug resistance and prevent relapse. Glasdegib is currently under investigation for select hematologic malignancies, including AML and MDS.

Along with our marketed products for hematological conditions, Pfizer is advancing a broad range of therapies that leverage select pathways and mechanisms of action to address acute and chronic leukemias, myeloproliferative disorders and lymphoma. In the near-term, Pfizer is in discussions with global regulatory authorities about inotuzumab ozogamicin for the treatment of acute lymphoblastic leukemia (ALL) and Mylotarg (gemtuzumab ozogamicin) for the treatment of acute myeloid leukemia (AML).

 
[Close]