CytoDyn announces data on mechanism of action of leronlimab

CytoDyn (CYDY) announced new data suggesting a novel mechanism of action of leronlimab for the treatment of solid tumors. CytoDyn analyzed data from its prior clinical trials of patients with metastatic Triple-Negative Breast Cancer and found that leronlimab treatment correlated with increased expression of an immune cell protein or “checkpoint inhibitor” known as programmed death-ligand 1 on patient’s circulating tumor cells. CytoDyn’s results indicate that 15/17 of patients who received a weekly dose of 525 mg or higher experienced a significant increase in PD-L1 expression on their CTCs over a 30-to-90-day period after starting leronlimab. Increasing expression of PD-L1 can be likened to turning “cold” tumors “hot”, elevating PD-L1 levels to the level necessary for patients to potentially derive benefit from further treatment with a class of drugs known as immune checkpoint inhibitors. As previously announced, CytoDyn identified a group of patients with mTNBC who had failed a median of two prior lines of treatment in the metastatic setting but showed improved overall survival rates after receiving leronlimab. The Company confirmed that 5/5 patients who demonstrated a significant increase in PD-L1 expression after receiving leronlimab and received treatment with any ICI remain alive today. Four of these patients currently identify as having no evidence of disease, and the fifth patient is alive and identified by the clinical site as “stable.” If the results above are confirmed prospectively, the Company believes the mechanism could be effective across a wide range of solid tumor types, and in particular benefit cancer patients with low levels of PD-L1 who were previously unresponsive to or ineligible for checkpoint inhibitors.