CytoDyn Presents at AACR Special Conference in Cancer Research: Brain Cancer
Preclinical data demonstrates leronlimab-mediated CCR5 inhibition enhances Temozolomide and radiation response in Glioblastoma
Leronlimab demonstrates synergy with standard-of-care therapies, supports plan for prospective combination study
VANCOUVER, Washington, March 24, 2026 (GLOBE NEWSWIRE) -- CytoDyn Inc. (OTCQB: CYDY) ("CytoDyn" or the "Company" ), a clinical-stage oncology company advancing leronlimab, a first-in-class humanized monoclonal antibody targeting the CCR5 receptor with therapeutic potential across multiple indications, including metastatic triple-negative breast cancer (“mTNBC”) and colorectal cancer (“mCRC”), today announced the presentation of new preclinical and translational data supporting the potential role of CCR5 inhibition in glioblastoma multiforme (GBM) at AACR Special Conference in Cancer Research: Brain Cancer, held March 23-25, in Philadelphia.
Glioblastoma multiforme (GBM) is an aggressive brain cancer with poor survival and limited effective treatment options. Standard therapies such as radiation and temozolomide (TMZ) often face resistance, and immune checkpoint inhibitors have shown limited benefit. Molecular profiling has shown that the tumor “core” of GBM is frequently characterized by a hypoxic, mesenchymal and immunosuppressive environment that contributes to treatment resistance. The data presented evaluate the role of CCR5 in these tumor core features and explore whether CCR5 inhibition with leronlimab may enhance responses to standard-of-care therapies.
“Our findings show that CCR5 expression correlates with glycolytic and hypoxic tumor core signatures, as well as markers of T-cell exhaustion,” said Professor Richard Pestell, M.D., Ph.D., FRCP, AO, Lead Consultant in Preclinical and Clinical Oncology at CytoDyn. “Importantly, CCR5 inhibition with leronlimab enhanced tumor cell killing when combined with temozolomide or radiation, support further clinical evaluation of leronlimab as a potential adjunct to standard-of-care therapy in glioblastoma.”
“These data, including the intriguing but preliminary results from a preclinical study in GBM, reinforce observations from other clinical and preclinical studies that demonstrate a striking impact of leronlimab in solid tumor oncology,” said Dr. Jacob Lalezari, M.D., Chief Executive Officer of CytoDyn. “These data outline a potential role for CCR5 in glioblastoma, where resistance to standard therapies remains a major unmet need. The observed synergy with temozolomide or radiation, combined with its association with immunosuppressive tumor core signatures, supports current plans to initiate a pilot study evaluating leronlimab in glioblastoma.”
Key findings:
In primary GBM tumors (N=154), CCR5 expression was significantly elevated compared to normal brain tissue and correlated with poor prognosis.
CCR5 expression aligned with tumor “core” rather than “leading edge” gene signatures and correlated with hallmarks of glycolysis, hypoxia, inflammatory response, and the mesenchymal (MES) GBM subtype.
CCR5 expression was associated with T-cell exhaustion markers (PD-1, PD-L1, TIM3, PTX3) and immune suppressive mediators including S100A4. Single-cell sequencing confirmed expression of CCR5 and its ligand CCL5 within the GBM tumor microenvironment and tumor glial metabolic subtypes.
In human GBM cell lines, CCR5 abundance increased upon neurosphere formation. CCR5 inhibition with leronlimab or maraviroc demonstrated functional synergy with temozolomide, enhancing tumor cell killing. Pretreatment with leronlimab also enhanced radiation-induced cytotoxicity.
Metabolic profiling using Seahorse analysis showed that CCR5 inhibition reduced oxygen consumption rate (OCR) in a dose-dependent manner, consistent with modulation of glycolytic and metabolic programs that contribute to an immunosuppressive tumor microenvironment.
The poster, titled “CCR5 inhibition with the human monoclonal antibody leronlimab enhances temozolomide- and radiation-induced killing of glioblastoma multiforme cells,” was presented by Ritika Harish on March 23, 2026, from 7:15 p.m. – 9:15 p.m. EDT (Poster #A002). A copy of the poster will be made available on CytoDyn’s website under the Publications & Posters section.”
Leronlimab has previously demonstrated a favorable safety profile in clinical studies and has been shown to cross the blood-brain barrier in non-human primate models. Together with encouraging long-term survival observations in metastatic breast cancer in combination immunotherapy settings, these findings support continued investigation of CCR5 blockade across solid tumor indications.
Preclinical data demonstrates leronlimab-mediated CCR5 inhibition enhances Temozolomide and radiation response in Glioblastoma
Leronlimab demonstrates synergy with standard-of-care therapies, supports plan for prospective combination study
VANCOUVER, Washington, March 24, 2026 (GLOBE NEWSWIRE) -- CytoDyn Inc. (OTCQB: CYDY) ("CytoDyn" or the "Company" ), a clinical-stage oncology company advancing leronlimab, a first-in-class humanized monoclonal antibody targeting the CCR5 receptor with therapeutic potential across multiple indications, including metastatic triple-negative breast cancer (“mTNBC”) and colorectal cancer (“mCRC”), today announced the presentation of new preclinical and translational data supporting the potential role of CCR5 inhibition in glioblastoma multiforme (GBM) at AACR Special Conference in Cancer Research: Brain Cancer, held March 23-25, in Philadelphia.
Glioblastoma multiforme (GBM) is an aggressive brain cancer with poor survival and limited effective treatment options. Standard therapies such as radiation and temozolomide (TMZ) often face resistance, and immune checkpoint inhibitors have shown limited benefit. Molecular profiling has shown that the tumor “core” of GBM is frequently characterized by a hypoxic, mesenchymal and immunosuppressive environment that contributes to treatment resistance. The data presented evaluate the role of CCR5 in these tumor core features and explore whether CCR5 inhibition with leronlimab may enhance responses to standard-of-care therapies.
“Our findings show that CCR5 expression correlates with glycolytic and hypoxic tumor core signatures, as well as markers of T-cell exhaustion,” said Professor Richard Pestell, M.D., Ph.D., FRCP, AO, Lead Consultant in Preclinical and Clinical Oncology at CytoDyn. “Importantly, CCR5 inhibition with leronlimab enhanced tumor cell killing when combined with temozolomide or radiation, support further clinical evaluation of leronlimab as a potential adjunct to standard-of-care therapy in glioblastoma.”
“These data, including the intriguing but preliminary results from a preclinical study in GBM, reinforce observations from other clinical and preclinical studies that demonstrate a striking impact of leronlimab in solid tumor oncology,” said Dr. Jacob Lalezari, M.D., Chief Executive Officer of CytoDyn. “These data outline a potential role for CCR5 in glioblastoma, where resistance to standard therapies remains a major unmet need. The observed synergy with temozolomide or radiation, combined with its association with immunosuppressive tumor core signatures, supports current plans to initiate a pilot study evaluating leronlimab in glioblastoma.”
Key findings:
In primary GBM tumors (N=154), CCR5 expression was significantly elevated compared to normal brain tissue and correlated with poor prognosis.
CCR5 expression aligned with tumor “core” rather than “leading edge” gene signatures and correlated with hallmarks of glycolysis, hypoxia, inflammatory response, and the mesenchymal (MES) GBM subtype.
CCR5 expression was associated with T-cell exhaustion markers (PD-1, PD-L1, TIM3, PTX3) and immune suppressive mediators including S100A4. Single-cell sequencing confirmed expression of CCR5 and its ligand CCL5 within the GBM tumor microenvironment and tumor glial metabolic subtypes.
In human GBM cell lines, CCR5 abundance increased upon neurosphere formation. CCR5 inhibition with leronlimab or maraviroc demonstrated functional synergy with temozolomide, enhancing tumor cell killing. Pretreatment with leronlimab also enhanced radiation-induced cytotoxicity.
Metabolic profiling using Seahorse analysis showed that CCR5 inhibition reduced oxygen consumption rate (OCR) in a dose-dependent manner, consistent with modulation of glycolytic and metabolic programs that contribute to an immunosuppressive tumor microenvironment.
The poster, titled “CCR5 inhibition with the human monoclonal antibody leronlimab enhances temozolomide- and radiation-induced killing of glioblastoma multiforme cells,” was presented by Ritika Harish on March 23, 2026, from 7:15 p.m. – 9:15 p.m. EDT (Poster #A002). A copy of the poster will be made available on CytoDyn’s website under the Publications & Posters section.”
Leronlimab has previously demonstrated a favorable safety profile in clinical studies and has been shown to cross the blood-brain barrier in non-human primate models. Together with encouraging long-term survival observations in metastatic breast cancer in combination immunotherapy settings, these findings support continued investigation of CCR5 blockade across solid tumor indications.
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