CytoDyn analyzed data from its prior clinical tria

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CytoDyn analyzed data from its prior clinical trials of patients with metastatic Triple-Negative Breast Cancer (“mTNBC”) and found that leronlimab treatment correlated with increased expression of an immune cell protein or “checkpoint inhibitor” known as programmed death-ligand 1 (“PD-L1”) on patient’s circulating tumor cells (“CTCs”). CytoDyn’s results indicate that 15/17 (88%) 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 (“ICIs”).

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 (100%) 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 (80%) currently identify as having no evidence of disease, and the fifth patient is alive and identified by the clinical site as “stable.”

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Very odd as maraviroc has been shown to downregulate PD-L1 by up to 80%.

Cold tumors are cold because there are less killer T-cells around the tumor. The expression of PD-L1 causes a hot tumor because elevation of PD-L1 is a response to killer T-cells that already exist around the tumor. Leronlimab would increase killer T-cells even with a cold tumor. With elevated killer T-cells from leronlimab around the tumor it would be preferential to not have elevated PD1/PD-L1 levels because there's no reason to block something that doesn't exist.