Micromet, Inc. (NASDAQ: MITI) today announced that it has initiated a phase 2 trial of its lead product candidate blinatumomab (MT103) in adult patients with relapsed or refractory (r/r) B-precursor acute lymphoblastic leukemia (ALL). Blinatumomab is the first of a new class of agents called BiTE® antibodies, designed to harness the body’s T cells to kill cancer cells.

This phase 2, single-arm study will evaluate the efficacy and safety of blinatumomab in approximately 65 patients with relapsed/refractory Philadelphia-negative B-precursor ALL. Patients will receive blinatumomab daily for 28 days followed by two weeks off blinatumomab over a six week treatment cycle. Patients who achieve a complete remission (CR) or complete response without full recovery of platelets (CRh*) within two cycles of treatment will receive up to three additional cycles of consolidation treatment. The primary endpoint of the study is CR/CRh*. Secondary endpoints include duration of response and overall survival. The study will be conducted at approximately 40 leading cancer centers in the U.S. and EU. The Company currently expects to complete enrollment in this trial by year end 2012.  » Read more...

In several clinical trials, antibody company Micromet has demonstrated outstanding efficacy and safety of its bispecific BiTE antibodies which come with two binding sites: one for a cancer target and a second one for a T cell. As a result, T cells are recruited and guided directly to the tumor cell, initiating cancer cell death in a serial fashion.

In this week’s PNAS, researchers of the company demonstrate that the BiTE antibodies also can overcome the notorious resistance against conventional monoclonal antibodies arising in many cancer patients.

The researchers converted the anti-EGFR antibodies cetuximab (Erbitux) and panitumumab (Vectibix) into BiTE antibodies by adding the binding site for T cells. In animal models, these BiTE antibodies then showed a remarkably high potency (in the sub-picomolar range) against cancer cells with KRAS and BRAF-mutations which made them resistant to the original monoclonal antibodies.  » Read more...