Interesting observation that leronlimab blocks CCL3 and CCL4 at CCR5 receptor, not just CCL5/RANTES.

Previous statement from Cytodyn (I've seen only in SEC filings without underlying research) stated selective inhibition of CCL5.

Jlang (thanks!) let me know that CCL3/4 blockade mentioned in this recent article.

https://breast-cancer-research.biomedcentral....21-01391-1

Quote:

---

Leronlimab blocks human CCL3- and CCL4-induced Ca+ 2 responses in human breast cancer cells
Other ligands such as CCL3 and CCL4 can also bind to CCR5. Leronlimab abrogated CCL3 (Fig. 3a, b) and CCL4 (Fig. 3c, d) induced Ca+ 2 flux in MDA-MB-231-CCR5 cells (Fig. 3).

---

IMO, blockade of all three will be beneficial to many patients.

Excerpt from one article highlighting the central role of CCL3 in autoimmune diseases. CCR5 inhibition is more than just blocking RANTES.

https://link.springer.com/referenceworkentry/...-7696-8_27

Quote:

---

Macrophage inflammatory protein-1 alpha (MIP-1α/CCL3) is a chemotactic chemokine secreted by macrophages. It performs various biological functions, such as recruiting inflammatory cells, wound healing, inhibition of stem cells, and maintaining effector immune response. It activates bone resorption cells and directly induces bone destruction. Cells that secrete MIP-1α/CCL3 are increased at sites of inflammation and bone resorption. MIP-1α/CCL3 plays an important role in the pathogenesis of various inflammatory diseases and conditions that exhibit bone resorption, such as periodontitis, multiple myeloma, Sjögren syndrome, and rheumatoid arthritis. Biological fluids from patients with these diseases exhibit elevated levels of MIP-1α/CCL3. This finding indicates that MIP-1

---