Trillium Therapeutics Provides Update on Its TTI-621 and TTI-622 Clinical Programs

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Trillium Therapeutics (Nasdaq:TRIL) a clinical stage immuno-oncology company developing innovative therapies for the treatment of cancer, today provided the following update on its TTI-621 and TTI-622 clinical programs. TTI-621 and TTI-622 target CD47, a protein commonly found on the surface of cancer cells. CD47 emits a “do not eat” signal to the immune system, allowing cancer cells …

Trillium Therapeutics (Nasdaq:TRIL) a clinical stage immuno-oncology company developing innovative therapies for the treatment of cancer, today provided the following update on its TTI-621 and TTI-622 clinical programs. TTI-621 and TTI-622 target CD47, a protein commonly found on the surface of cancer cells. CD47 emits a “do not eat” signal to the immune system, allowing cancer cells to evade detection.

As quoted in the press release:

TTI-621 (SIRPa-IgG1 Fc) is a decoy receptor that blocks CD47 and delivers an activating signal to effector cells such as macrophages through its IgG1 Fc region. It is being evaluated in two multi-center clinical trials using intravenous or intratumoral administration and preliminary data from both studies were reported at last year’s American Society of Hematology Annual Meeting. Notably, weekly infusions of TTI-621 were shown to be well tolerated and intratumoral injection was observed to reduce local lesions in 9 out of 10 patients with mycosis fungoides, a common type of cutaneous T-cell lymphoma (CTCL). Building upon these monotherapy results, Trillium has refined and focused its TTI-621 clinical program.

“Our thorough signal-seeking efforts in the TTI-621 program have successfully identified T-cell lymphoma as an indication of interest,” said Dr. Niclas Stiernholm, President and CEO of Trillium Therapeutics. “Consequently, we are now moving forward with a more focused TTI-621 program that reflects our commitment to vigorously pursue this signal in both the intravenous and intratumoral trials.”

Click here to read the full press release.

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