- Administration of expanded human Tregs with amplified immunomodulatory function suppressed neuroinflammation and alleviated AD pathology in a mice model of AD.
- Expanded human Tregs reduced amyloid burden and downregulated neuroinflammatory markers in the brain including pro-inflammatory cytokines, complement cascade, toll like receptors, and microglia.
- Data provide preclinical support for Treg enhancing therapies as a potential treatment strategy in AD and other neurodegenerative diseases.
- Initiation of Phase I clinical trials for Treg enhancing biologics in neurodegenerative diseases expected in 2023 with interim data readout by or before Q1 2024.
HOUSTON, TX, USA I January 26, 2023 ICoya Therapeutics, Inc. (NASDAQ: COYA) (“Coya” or the “Company”), a clinical-stage biotechnology company developing multiple therapeutic platforms that enhance Treg function, including biologics and cell therapies, announced the recent publication of an article entitled “Ex vivo expanded human regulatory T cells modify neuroinflammation in a preclinical model of Alzheimer’s Disease” in the peer reviewed journal Acta Neuropathologica Communications. The preclinical study was conducted by Ali Faridar, M.D., of Houston Methodist Hospital (Houston, Texas), under the leadership of Stanley Appel, M.D., the chair of Coya’s Scientific Advisory Board.
“These data further support that enhancing Treg function is a potential strategy to ameliorate neuroinflammation, which may modify Alzheimer’s Disease-associated pathology in the brain. Coya intends to enter a Phase I clinical trial of Treg enhancing biologics for the treatment of neurodegenerative diseases in 2023 with interim data readout anticipated by or before Q1 2024,” stated Howard Berman, Ph.D., Chief Executive Officer of Coya. “We continue advancing our product candidate pipeline including our biologic programs, which are intended to enhance Treg function in vivo and we believe have the potential to address the significant unmet needs of patients with serious neurodegenerative diseases,” stated Dr. Berman.
Stanley Appel, MD., Professor, Houston Methodist Hospital and Chair of Coya’s Scientific Advisory Board, commented, “Dr. Faridar’s transgenic mouse model study provides compelling evidence for the neuroprotective role of Tregs in suppressing neuroinflammation to improve disease pathophysiology and supports the potential role of immunomodulatory therapy for patients with AD and other neurodegenerative diseases.”
The study investigated the therapeutic effects of ex vivo expanded human Tregs on 5xFAD immunodeficient mice (5xFAD-Rag2KO), a well characterized model of AD. Treg administration reduced the levels of both soluble and insoluble Aβ40 and Aβ42 in the dentate gyrus and frontal cortex of treated animals compared to controls. Furthermore, Treg-treated mice showed significant reduction in total and plaque-associated microglia as well as reactive astrocytes in dentate gyrus and frontal cortex versus untreated mice.
Consistent with these findings, proteomic evaluation of the neuroinflammation transcriptome revealed that Treg administration down regulated multiple inflammatory pathways that have been observed to be associated with toxic amyloid beta (Aβ) including pro-inflammatory cytokines (IL1A&B, IL6), complement cascade (C1qa, C1qb, C4a/b), toll like receptors (Tlr3, Tlr4 and Tlr7) and microglial activations markers (CD14, Tyrobp, Trem2). The reduction in the number of plaque-associated glial cells and suppression of pro-inflammatory signaling pathways within these cells following Treg therapy may attenuate the contribution of these toxic glial cells in AD pathology resulting in mitigation of amyloid burden.
The peer reviewed publication can be accessed at https://actaneurocomms.biomedcentral.com/articles/10.1186/s40478-022-01447-z
About Coya Therapeutics, Inc.
Headquartered in Houston, TX, Coya Therapeutics, Inc. (Nasdaq: COYA) is a clinical-stage biotechnology company developing proprietary treatments focused on the biology and potential therapeutic advantages of regulatory T cells (“Tregs”) to target systemic inflammation and neuroinflammation. Dysfunctional Tregs underlie numerous conditions including neurodegenerative, metabolic, and autoimmune diseases, and this cellular dysfunction may lead to a sustained inflammation and oxidative stress resulting in lack of homeostasis of the immune system. Coya’s investigational product candidate pipeline leverages multiple therapeutic modalities aimed at restoring the anti-inflammatory and immunomodulatory functions of Tregs. Coya’s therapeutic platforms include Treg-enhancing biologics, Treg-derived exosomes, and autologous Treg cell therapy. Coya’s 300 Series product candidates, COYA 301 and COYA 302, are biologic therapies intended to enhance Treg function and expand Treg numbers. COYA 301 is a cytokine biologic for subcutaneous administration intended to enhance Treg function and expand Treg numbers in vivo, and COYA 302 is a biologic combination for subcutaneous and/or intravenous administration intended to enhance Treg function while depleting T effector function and activated macrophages. These two mechanisms may be additive or synergistic in suppressing inflammation. For more information about Coya, please visit www.coyatherapeutics.com.
SOURCE: Coya Therapeutics
Post Views: 24
- Administration of expanded human Tregs with amplified immunomodulatory function suppressed neuroinflammation and alleviated AD pathology in a mice model of AD.
- Expanded human Tregs reduced amyloid burden and downregulated neuroinflammatory markers in the brain including pro-inflammatory cytokines, complement cascade, toll like receptors, and microglia.
- Data provide preclinical support for Treg enhancing therapies as a potential treatment strategy in AD and other neurodegenerative diseases.
- Initiation of Phase I clinical trials for Treg enhancing biologics in neurodegenerative diseases expected in 2023 with interim data readout by or before Q1 2024.
HOUSTON, TX, USA I January 26, 2023 ICoya Therapeutics, Inc. (NASDAQ: COYA) (“Coya” or the “Company”), a clinical-stage biotechnology company developing multiple therapeutic platforms that enhance Treg function, including biologics and cell therapies, announced the recent publication of an article entitled “Ex vivo expanded human regulatory T cells modify neuroinflammation in a preclinical model of Alzheimer’s Disease” in the peer reviewed journal Acta Neuropathologica Communications. The preclinical study was conducted by Ali Faridar, M.D., of Houston Methodist Hospital (Houston, Texas), under the leadership of Stanley Appel, M.D., the chair of Coya’s Scientific Advisory Board.
“These data further support that enhancing Treg function is a potential strategy to ameliorate neuroinflammation, which may modify Alzheimer’s Disease-associated pathology in the brain. Coya intends to enter a Phase I clinical trial of Treg enhancing biologics for the treatment of neurodegenerative diseases in 2023 with interim data readout anticipated by or before Q1 2024,” stated Howard Berman, Ph.D., Chief Executive Officer of Coya. “We continue advancing our product candidate pipeline including our biologic programs, which are intended to enhance Treg function in vivo and we believe have the potential to address the significant unmet needs of patients with serious neurodegenerative diseases,” stated Dr. Berman.
Stanley Appel, MD., Professor, Houston Methodist Hospital and Chair of Coya’s Scientific Advisory Board, commented, “Dr. Faridar’s transgenic mouse model study provides compelling evidence for the neuroprotective role of Tregs in suppressing neuroinflammation to improve disease pathophysiology and supports the potential role of immunomodulatory therapy for patients with AD and other neurodegenerative diseases.”
The study investigated the therapeutic effects of ex vivo expanded human Tregs on 5xFAD immunodeficient mice (5xFAD-Rag2KO), a well characterized model of AD. Treg administration reduced the levels of both soluble and insoluble Aβ40 and Aβ42 in the dentate gyrus and frontal cortex of treated animals compared to controls. Furthermore, Treg-treated mice showed significant reduction in total and plaque-associated microglia as well as reactive astrocytes in dentate gyrus and frontal cortex versus untreated mice.
Consistent with these findings, proteomic evaluation of the neuroinflammation transcriptome revealed that Treg administration down regulated multiple inflammatory pathways that have been observed to be associated with toxic amyloid beta (Aβ) including pro-inflammatory cytokines (IL1A&B, IL6), complement cascade (C1qa, C1qb, C4a/b), toll like receptors (Tlr3, Tlr4 and Tlr7) and microglial activations markers (CD14, Tyrobp, Trem2). The reduction in the number of plaque-associated glial cells and suppression of pro-inflammatory signaling pathways within these cells following Treg therapy may attenuate the contribution of these toxic glial cells in AD pathology resulting in mitigation of amyloid burden.
The peer reviewed publication can be accessed at https://actaneurocomms.biomedcentral.com/articles/10.1186/s40478-022-01447-z
About Coya Therapeutics, Inc.
Headquartered in Houston, TX, Coya Therapeutics, Inc. (Nasdaq: COYA) is a clinical-stage biotechnology company developing proprietary treatments focused on the biology and potential therapeutic advantages of regulatory T cells (“Tregs”) to target systemic inflammation and neuroinflammation. Dysfunctional Tregs underlie numerous conditions including neurodegenerative, metabolic, and autoimmune diseases, and this cellular dysfunction may lead to a sustained inflammation and oxidative stress resulting in lack of homeostasis of the immune system. Coya’s investigational product candidate pipeline leverages multiple therapeutic modalities aimed at restoring the anti-inflammatory and immunomodulatory functions of Tregs. Coya’s therapeutic platforms include Treg-enhancing biologics, Treg-derived exosomes, and autologous Treg cell therapy. Coya’s 300 Series product candidates, COYA 301 and COYA 302, are biologic therapies intended to enhance Treg function and expand Treg numbers. COYA 301 is a cytokine biologic for subcutaneous administration intended to enhance Treg function and expand Treg numbers in vivo, and COYA 302 is a biologic combination for subcutaneous and/or intravenous administration intended to enhance Treg function while depleting T effector function and activated macrophages. These two mechanisms may be additive or synergistic in suppressing inflammation. For more information about Coya, please visit www.coyatherapeutics.com.
SOURCE: Coya Therapeutics
Post Views: 24
