EIND: Information to Submit to Doctors
Leronlimab a humanized monoclonal antibody binds CCR5, blocking binding of it's C-C chemokine ligands (preferentially binding CCL-4 and CCL-5). Leronlimab switches M2 (tumor protectant) macrophages to an M1 (immune responsive) macrophage type. Leronlimab downregulates both the PI3K/AKT/mTOR, MAPK/ERK pathways and VEGF(pro-angiogenesis). Leronlimab also reduces the immunosuppressive mediators sB7-H3, BAFF and sTyro3. The optimal dosage to date has been the 700mg dose. Leronlimab often greatly increases PD-L1 (tumor protectant) in response to the M1 macrophage shift and PD-L1 inhibitor administration is warranted in these circumstances.
Contact Information
Website - www.cytodyn.com
Phone - 360-980-8524
Email - info@cytodyn.com
Cytodyn welcomes all requests for the use of it's drug leronlimab under the FDA's Emergency Investigational New Drug Program. The preferred method of contact by physicians or patients is through Cytodyn's email address. Cytodyn will respond with more information about the drug and the steps to take to initiate the EIND process.
Online Links to Publications
Leronlimab is associated with long-term survival in metastatic TNBC: Enhancing PD-L1 expression, ICI response, and modulates T cell exhaustion
Abstract - https://aacrjournals.org/cancerimmunolres/art...-with-long
Poster - https://d1io3yog0oux5.cloudfront.net/_976f96f...evised.pdf
Prolonged survival following PD-L1/PD-1 immune checkpoint inhibitor therapy after leronlimab induced PD-L1 upregulation on cancer-associated macrophage-like cells and circulating tumor cells in patients with metastatic or locally advanced triple-negative breast cancer
Abstract - https://aacrjournals.org/clincancerres/articl...llowing-PD
Poster - https://d1io3yog0oux5.cloudfront.net/_fb000f7..._FINAL.pdf
Long Term Survival with Leronlimab Treatment in Patients with Metastatic Triple-Negative Breast Cancer (mTNBC)
Poster - https://d1io3yog0oux5.cloudfront.net/_976f96f...28h%29.pdf
Leronlimab induces PD-L1 expression and is associated with long‑term survival with an ICI in PD-L1 low metastatic TNBC
Abstract (for April 19, 2026 presentation) - https://www.abstractsonline.com/pp8/#!/21436/...ation/9742
Leronlimab, a humanized monoclonal antibody to CCR5, blocks breast cancer cellular metastasis and enhances cell death induced by DNA damaging chemotherapy
Publication - https://link.springer.com/article/10.1186/s13058-021-01391-1
Leronlimab induces PD-L1 expression and is associated with long-term survival with an ICI in PD-L1 low metastatic TNBC
https://d1io3yog0oux5.cloudfront.net/_8fabbae...P+3-21.pdf
Leronlimab in combination with trifluridine/tipiracil (TAS-102) plus bevacizumab for patients with
refractory metastatic colorectal cancer (mCRC): The phase 2 CLOVER study
https://d1io3yog0oux5.cloudfront.net/_bda4625...026_V6.pdf
The Role and Therapeutic Targeting of CCR5 in Breast Cancer
Publication - https://pdfs.semanticscholar.org/c499/b3b8f8d...32aa89.pdf
The CCL5/CCR5 Axis in Cancer Progression
Publication - https://www.mdpi.com/2072-6694/12/7/1765
``````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````
Progesterone +. Estrogen+, specific information
Leronlimab a humanized monoclonal antibody binds CCR5, blocking binding of it's C-C chemokine ligands (preferentially binding CCL-4 and CCL-5). Leronlimab downregulates both the PI3K/AKT/mTOR and MAPK/ERK pathways.
CCL5/CCR5 axis in human diseases and related treatments
"CCL5/CCR5 axis focus on influencing the cell cycle of tumor cells through abnormally activating NF-κB, mTOR and PI3K/AKT signaling pathways. At the molecular level, the cell division-related genes like cyclin D1, c-Myc and Dad-1 are overexpressed at tumor cell surface. They cooperate with each other to strengthen the mitogenesis. Furthermore, mTOR-mediated glycolysis and ATP production provide sufficient energy for the growth of tumor cells. In this process, CCL5/CCR5 combination triggers mTOR signaling continuously for cell proliferation."
https://pmc.ncbi.nlm.nih.gov/articles/PMC8423937/
The Inflammatory Chemokine CCL5 and Cancer Progression
"More specifically, CCL5 contributes to the activation of the αvβ3 integrin and to cell migration through PI3K/Akt, which in turn activates IKKalpha/beta and NF-κB. NF-κB activation also can elevate the secretion of MMP-9 or promote invasion by increasing the secretion of both MMP-2 and -9 and by activating the ERK and Rac signaling [27]. CCL5 induces migration also by upregulating the activities of MMP-9 through STAT3 [28]. In other instances CCL5/CCR5 acts via MEK, ERK, and then NF-κB, resulting in the activations of αvβ3 integrin and contributing to cell migration.
Chemokines, by activating the tyrosine kinase receptors, the Jak-STAT, or the MAPK/ERK signaling pathway, also promote tumor cell proliferation. Exogenous CCL5 stimulates cell proliferation by inducing the mTOR pathway, leading to a rapid upregulation of cyclin D1, c-Myc, and Dad-1 expression. An additional mechanism based on the CCL5-CCR5 interaction can lead to increased cell proliferation: increased glucose uptake, increased ATP production, and enhanced glycolysis, associated with extracellular acidification"
https://onlinelibrary.wiley.com/doi/10.1155/2014/292376
````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````
Endocrine therapy resistance in breast cancer: current status, possible mechanisms and overcoming strategies
"Endocrine therapy combined with mTOR inhibitors
The PI3K–AKT–mTOR pathway has also been implicated to play a crucial role in tumor proliferation and progression. Several studies showed that the upregulation of the PI3K–AKT–mTOR pathway interacts with the ER pathway and confers endocrine resistance... Another preclinical study showed that co-treatment with low concentrations of mTOR inhibitor RAD001 combining with either letrozole or fulvestrant could restore the response of the resistant cells with high Akt activity. In addition, it could also resensitize breast cancer cells that did not respond to letrozole or fulvestrant as a single agent"
https://pmc.ncbi.nlm.nih.gov/articles/PMC5558537/
The role of the tumor microenvironment in endocrine therapy resistance in hormone receptor-positive breast cancer
"The MAPK/ERK pathway is one of the most classical intracellular signaling pathways which is involved in tumor progression and drug resistance. The activation of the MAPK/ERK signaling axis phosphorylates ER, increases the sensitivity of ER to estrogen, and thereby contributes to endocrine therapy resistance. In addition, it communicates with other signaling pathways and cooperates to promote the proliferation and migration of tumor cells."
https://pmc.ncbi.nlm.nih.gov/articles/PMC10611521/#s7
`````````````````````````````````````````````````````````````````````````````````````````````````````
Leronlimab, CCR5 and Glioblastoma
CCR5 inhibition with the human monoclonal antibody leronlimab enhances temozolomide- and radiation-induced killing of glioblastoma multiforme cells
Abstract - https://aacrjournals.org/cancerres/article/86...-the-human
Poster - https://d1io3yog0oux5.cloudfront.net/_65e5c24...poster.pdf
`````````````````````````````````````````````````````````````````````````````````````````````````````
Critical roles of chemokine receptor CCR5 in regulating glioblastoma proliferation and invasion
https://academic.oup.com/abbs/article/47/11/890/1412
Blockade of CCR5 receptor prevents M2 microglia phenotype in a microglia-glioma paradigm
https://www.sciencedirect.com/science/article...8617300724
Cytokine CCL5 and receptor CCR5 axis in glioblastoma multiforme
https://reference-global.com/download/article...9-0057.pdf
CCR5-Mediated Signaling is Involved in Invasion of Glioblastoma Cells in Its Microenvironment
https://www.mdpi.com/1422-0067/21/12/4199
An Update on Glioblastoma Biology, Genetics, and Current Therapies: Novel Inhibitors of the G Protein-Coupled Receptor CCR5
https://www.mdpi.com/1422-0067/22/9/4464#
Reactive oligodendrocytes promote glioblastoma progression through CCL5/CCR5-mediated glioma stem cell maintenance
https://www.sciencedirect.com/science/article...7325009390
Leronlimab a humanized monoclonal antibody binds CCR5, blocking binding of it's C-C chemokine ligands (preferentially binding CCL-4 and CCL-5). Leronlimab switches M2 (tumor protectant) macrophages to an M1 (immune responsive) macrophage type. Leronlimab downregulates both the PI3K/AKT/mTOR, MAPK/ERK pathways and VEGF(pro-angiogenesis). Leronlimab also reduces the immunosuppressive mediators sB7-H3, BAFF and sTyro3. The optimal dosage to date has been the 700mg dose. Leronlimab often greatly increases PD-L1 (tumor protectant) in response to the M1 macrophage shift and PD-L1 inhibitor administration is warranted in these circumstances.
Contact Information
Website - www.cytodyn.com
Phone - 360-980-8524
Email - info@cytodyn.com
Cytodyn welcomes all requests for the use of it's drug leronlimab under the FDA's Emergency Investigational New Drug Program. The preferred method of contact by physicians or patients is through Cytodyn's email address. Cytodyn will respond with more information about the drug and the steps to take to initiate the EIND process.
Online Links to Publications
Leronlimab is associated with long-term survival in metastatic TNBC: Enhancing PD-L1 expression, ICI response, and modulates T cell exhaustion
Abstract - https://aacrjournals.org/cancerimmunolres/art...-with-long
Poster - https://d1io3yog0oux5.cloudfront.net/_976f96f...evised.pdf
Prolonged survival following PD-L1/PD-1 immune checkpoint inhibitor therapy after leronlimab induced PD-L1 upregulation on cancer-associated macrophage-like cells and circulating tumor cells in patients with metastatic or locally advanced triple-negative breast cancer
Abstract - https://aacrjournals.org/clincancerres/articl...llowing-PD
Poster - https://d1io3yog0oux5.cloudfront.net/_fb000f7..._FINAL.pdf
Long Term Survival with Leronlimab Treatment in Patients with Metastatic Triple-Negative Breast Cancer (mTNBC)
Poster - https://d1io3yog0oux5.cloudfront.net/_976f96f...28h%29.pdf
Leronlimab induces PD-L1 expression and is associated with long‑term survival with an ICI in PD-L1 low metastatic TNBC
Abstract (for April 19, 2026 presentation) - https://www.abstractsonline.com/pp8/#!/21436/...ation/9742
Leronlimab, a humanized monoclonal antibody to CCR5, blocks breast cancer cellular metastasis and enhances cell death induced by DNA damaging chemotherapy
Publication - https://link.springer.com/article/10.1186/s13058-021-01391-1
Leronlimab induces PD-L1 expression and is associated with long-term survival with an ICI in PD-L1 low metastatic TNBC
https://d1io3yog0oux5.cloudfront.net/_8fabbae...P+3-21.pdf
Leronlimab in combination with trifluridine/tipiracil (TAS-102) plus bevacizumab for patients with
refractory metastatic colorectal cancer (mCRC): The phase 2 CLOVER study
https://d1io3yog0oux5.cloudfront.net/_bda4625...026_V6.pdf
The Role and Therapeutic Targeting of CCR5 in Breast Cancer
Publication - https://pdfs.semanticscholar.org/c499/b3b8f8d...32aa89.pdf
The CCL5/CCR5 Axis in Cancer Progression
Publication - https://www.mdpi.com/2072-6694/12/7/1765
``````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````
Progesterone +. Estrogen+, specific information
Leronlimab a humanized monoclonal antibody binds CCR5, blocking binding of it's C-C chemokine ligands (preferentially binding CCL-4 and CCL-5). Leronlimab downregulates both the PI3K/AKT/mTOR and MAPK/ERK pathways.
CCL5/CCR5 axis in human diseases and related treatments
"CCL5/CCR5 axis focus on influencing the cell cycle of tumor cells through abnormally activating NF-κB, mTOR and PI3K/AKT signaling pathways. At the molecular level, the cell division-related genes like cyclin D1, c-Myc and Dad-1 are overexpressed at tumor cell surface. They cooperate with each other to strengthen the mitogenesis. Furthermore, mTOR-mediated glycolysis and ATP production provide sufficient energy for the growth of tumor cells. In this process, CCL5/CCR5 combination triggers mTOR signaling continuously for cell proliferation."
https://pmc.ncbi.nlm.nih.gov/articles/PMC8423937/
The Inflammatory Chemokine CCL5 and Cancer Progression
"More specifically, CCL5 contributes to the activation of the αvβ3 integrin and to cell migration through PI3K/Akt, which in turn activates IKKalpha/beta and NF-κB. NF-κB activation also can elevate the secretion of MMP-9 or promote invasion by increasing the secretion of both MMP-2 and -9 and by activating the ERK and Rac signaling [27]. CCL5 induces migration also by upregulating the activities of MMP-9 through STAT3 [28]. In other instances CCL5/CCR5 acts via MEK, ERK, and then NF-κB, resulting in the activations of αvβ3 integrin and contributing to cell migration.
Chemokines, by activating the tyrosine kinase receptors, the Jak-STAT, or the MAPK/ERK signaling pathway, also promote tumor cell proliferation. Exogenous CCL5 stimulates cell proliferation by inducing the mTOR pathway, leading to a rapid upregulation of cyclin D1, c-Myc, and Dad-1 expression. An additional mechanism based on the CCL5-CCR5 interaction can lead to increased cell proliferation: increased glucose uptake, increased ATP production, and enhanced glycolysis, associated with extracellular acidification"
https://onlinelibrary.wiley.com/doi/10.1155/2014/292376
````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````
Endocrine therapy resistance in breast cancer: current status, possible mechanisms and overcoming strategies
"Endocrine therapy combined with mTOR inhibitors
The PI3K–AKT–mTOR pathway has also been implicated to play a crucial role in tumor proliferation and progression. Several studies showed that the upregulation of the PI3K–AKT–mTOR pathway interacts with the ER pathway and confers endocrine resistance... Another preclinical study showed that co-treatment with low concentrations of mTOR inhibitor RAD001 combining with either letrozole or fulvestrant could restore the response of the resistant cells with high Akt activity. In addition, it could also resensitize breast cancer cells that did not respond to letrozole or fulvestrant as a single agent"
https://pmc.ncbi.nlm.nih.gov/articles/PMC5558537/
The role of the tumor microenvironment in endocrine therapy resistance in hormone receptor-positive breast cancer
"The MAPK/ERK pathway is one of the most classical intracellular signaling pathways which is involved in tumor progression and drug resistance. The activation of the MAPK/ERK signaling axis phosphorylates ER, increases the sensitivity of ER to estrogen, and thereby contributes to endocrine therapy resistance. In addition, it communicates with other signaling pathways and cooperates to promote the proliferation and migration of tumor cells."
https://pmc.ncbi.nlm.nih.gov/articles/PMC10611521/#s7
`````````````````````````````````````````````````````````````````````````````````````````````````````
Leronlimab, CCR5 and Glioblastoma
CCR5 inhibition with the human monoclonal antibody leronlimab enhances temozolomide- and radiation-induced killing of glioblastoma multiforme cells
Abstract - https://aacrjournals.org/cancerres/article/86...-the-human
Poster - https://d1io3yog0oux5.cloudfront.net/_65e5c24...poster.pdf
`````````````````````````````````````````````````````````````````````````````````````````````````````
Critical roles of chemokine receptor CCR5 in regulating glioblastoma proliferation and invasion
https://academic.oup.com/abbs/article/47/11/890/1412
Blockade of CCR5 receptor prevents M2 microglia phenotype in a microglia-glioma paradigm
https://www.sciencedirect.com/science/article...8617300724
Cytokine CCL5 and receptor CCR5 axis in glioblastoma multiforme
https://reference-global.com/download/article...9-0057.pdf
CCR5-Mediated Signaling is Involved in Invasion of Glioblastoma Cells in Its Microenvironment
https://www.mdpi.com/1422-0067/21/12/4199
An Update on Glioblastoma Biology, Genetics, and Current Therapies: Novel Inhibitors of the G Protein-Coupled Receptor CCR5
https://www.mdpi.com/1422-0067/22/9/4464#
Reactive oligodendrocytes promote glioblastoma progression through CCL5/CCR5-mediated glioma stem cell maintenance
https://www.sciencedirect.com/science/article...7325009390
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