CDC42 inhibition stem cell rejuvenation platform
preclinicalplatform · high · Wed Oct 26 2022 00:00:00 GMT+0000 (Coordinated Universal Time)
Develop pharmacological approaches to rejuvenate aged and exhausted stem cells by normalizing age-associated CDC42 overactivation and restoring cellular architecture and function, especially in hematopoietic stem cells.
Small-molecule CDC42 inhibition, including CASIN-associated research, to restore stem cell polarity, cytoskeletal organization, mitochondrial quality, and functional output.
Completed first seed investment round with Kizoo Technology Capital as sole investor on 2022-10-26.
Company materials state the platform targets elevated CDC42 activity associated with aging and aims to restore aged stem cell function; listed publications support effects across hematopoietic stem cells, bone, immune, skin, cancer, and neurodegeneration models.
Aged hematopoietic stem cell immune remodeling program
exploratoryresearch program · medium
Understand and potentially reverse aging-associated immune remodeling driven by aged hematopoietic stem cells.
Hematopoietic stem cell aging research focused on immune remodeling and stem-cell intrinsic/extrinsic rejuvenation mechanisms.
Mogling Bio listed publications titled “Aged murine hematopoietic stem cells drive aging-associated immune remodeling” and “Rejuvenation of Tissue Stem Cells by Intrinsic and Extrinsic Factors.”
Publication titles indicate aged murine hematopoietic stem cells drive immune remodeling and that tissue stem cell rejuvenation can involve intrinsic and extrinsic factors.
CASIN osteoporosis prevention program
preclinicaldrug program · high
Prevent or reverse age-associated osteoporosis and bone-remodeling dysfunction by inhibiting CDC42/Cdc42.
Mid-life CDC42 inhibition with CASIN/Cdc42 inhibitor treatment in normally aging mice and related osteoporosis models.
Preclinical publications listed for normally aging mice and conditioning-induced osteoporosis after stem-cell transplantation.
Publication titles indicate CASIN prevented osteoporosis in normally aging mice and Cdc42 inhibition prevented conditioning-induced osteoporosis after stem-cell transplantation.
Cdc42 inhibition cell rejuvenation platform
preclinicalplatform · high
Restore function in aged and exhausted cells, especially stem cells, by addressing age-associated Cdc42 overactivation for age-related diseases including osteoporosis, immune dysfunction, blood disorders, and neurodegeneration.
Pharmacological targeting of Cdc42 overactivation, including CASIN/Cdc42 inhibition approaches, to rejuvenate cell function.
Seed-stage company developing pharmacological Cdc42-targeted therapies; supporting publications listed across multiple disease models.
Supplied evidence reports Cdc42 inhibition or targeting across aged stem cells, osteoporosis, Parkinson's disease mice, skin aging, immune dysfunction, leukemia, multiple myeloma, and antitumor T-cell immunity.
Cdc42 inhibition for aged NK cell cytotoxic function
exploratoryresearch program · medium
Investigate whether Cdc42 overactivation contributes to impaired natural killer cell cytotoxicity in old individuals against senescent fibroblasts.
Study of Cdc42 GTPase overactivation and NK-cell cytotoxic function in old individuals.
Mogling Bio lists a publication on Cdc42 GTPase overactivation impairing cytotoxic function of NK cells from old individuals toward senescent fibroblasts.
The listed publication title reports that Cdc42 GTPase overactivation impairs NK-cell cytotoxic function in old individuals.
CDC42 inhibition for immune dysfunction and NK cell cytotoxicity
exploratoryresearch program · medium
Address age-associated immune dysfunction by reducing CDC42 overactivation and improving immune cell function against senescent cells.
CDC42-focused immune research in aged NK cells and regulatory T cells, including assessment of NK cytotoxicity toward senescent fibroblasts and antitumor T-cell immunity after CDC42 targeting.
Mogling Bio listed publications on CDC42 overactivation impairing aged NK cell cytotoxicity and CDC42 targeting in regulatory T cells unleashing antitumor T-cell immunity.
Publication titles indicate CDC42 overactivation impairs NK-cell cytotoxic function in old individuals, while CDC42 targeting in regulatory T cells enhances antitumor T-cell immunity.
Cdc42 inhibition for osteoporosis prevention
preclinicaldrug program · high
Prevent or reduce osteoporosis associated with aging or stem-cell transplantation conditioning by targeting Cdc42-driven cellular aging mechanisms.
Pharmacological Cdc42 inhibition with CASin/CASIN in mouse models of normal aging and conditioning-induced osteoporosis.
Multiple preclinical publications listed by Mogling Bio on Cdc42 inhibition preventing osteoporosis in aging mice and after stem-cell transplantation conditioning.
Publication titles report that Cdc42 inhibition prevents conditioning-induced osteoporosis after stem-cell transplantation and that mid-life CDC42 inhibition restores bone-remodeling cells, cytoskeletal architecture, and mitochondrial quality to prevent osteoporosis in aging.
CDC42 inhibition for osteoporosis prevention
preclinicaldrug program · high
Prevent or treat osteoporosis associated with aging or stem-cell transplantation conditioning by restoring bone remodeling cell function through CDC42 inhibition.
CDC42 inhibition with CASIN in mouse osteoporosis-related studies, including normally aging mice and conditioning-induced osteoporosis after stem-cell transplantation.
Mogling Bio listed a 2025 publication titled “Mid-life CDC42 inhibition restores cells of bone remodelling, cytoskeletal architecture and mitochondrial quality to prevent osteoporosis in ageing.”
Listed results indicate CASIN/CDC42 inhibition prevented osteoporosis in normally aging mice and conditioning-induced osteoporosis after stem-cell transplantation.
Cdc42 inhibition for Parkinson's disease motor phenotype
preclinicalresearch program · medium
Assess whether targeting Cdc42 can improve Parkinson's disease-related motor phenotypes and clarify age-dependent susceptibility to alpha-synuclein.
Cdc42-targeted intervention in Parkinson's disease mouse models involving alpha-synuclein susceptibility.
Mogling Bio lists a publication titled “Targeting Cdc42 improves motor phenotype in Parkinson’s disease mice and reveals age-dependent susceptibility to alpha-synuclein.”
The listed publication title reports improved motor phenotype in Parkinson's disease mice after targeting Cdc42.
CDC42 inhibition for Parkinson’s disease motor phenotype
preclinicalresearch program · medium
Improve Parkinson’s disease-related motor phenotypes and investigate age-dependent susceptibility to alpha-synuclein through CDC42 targeting.
CDC42-targeting intervention in Parkinson’s disease mouse models involving alpha-synuclein susceptibility.
Mogling Bio listed the publication “Targeting Cdc42 improves motor phenotype in Parkinson’s disease mice and reveals age-dependent susceptibility to alpha-synuclein.”
The publication title reports improved motor phenotype in Parkinson’s disease mice and age-dependent susceptibility to alpha-synuclein after CDC42 targeting.
Cdc42 inhibition for skin aging
preclinicalresearch program · medium
Evaluate anti-aging effects of Cdc42 inhibition on naturally aging skin.
Cdc42 inhibition in naturally aging mouse skin models.
Mogling Bio lists a publication titled “Cdc 42 inhibition exerts antiaging-effects on the skin of naturally aging mice.”
The listed publication title reports anti-aging effects on skin of naturally aging mice after Cdc42 inhibition.
CDC42 inhibition for skin aging
preclinicalresearch program · medium
Evaluate anti-aging effects of CDC42 inhibition in naturally aging skin.
CDC42 inhibition in naturally aging mouse skin models.
Mogling Bio listed the publication “Cdc 42 inhibition exerts antiaging-effects on the skin of naturally aging mice.”
The publication title reports anti-aging effects on the skin of naturally aging mice after CDC42 inhibition.
Cdc42 inhibition Parkinson's disease motor phenotype program
preclinicaldrug program · medium
Improve motor phenotype in Parkinson's disease and address age-dependent susceptibility to alpha-synuclein.
Cdc42 targeting/inhibition in Parkinson's disease mouse models.
Preclinical publication listed on targeting Cdc42 in Parkinson's disease mice.
Publication title states that targeting Cdc42 improved motor phenotype in Parkinson's disease mice and revealed age-dependent susceptibility to alpha-synuclein.
Cdc42 inhibition skin aging program
preclinicaldrug program · medium
Produce anti-aging effects in aged skin.
Cdc42 inhibition in naturally aging mouse skin models.
Preclinical publication listed for anti-aging effects on skin of naturally aging mice.
Publication title states that Cdc42 inhibition exerted anti-aging effects on the skin of naturally aging mice.
Cdc42 inhibition stem cell rejuvenation platform
preclinicalplatform · high
Develop pharmacological therapies that reduce age-associated Cdc42 overactivation to restore function in aged and exhausted cells, especially hematopoietic stem cells.
Small-molecule Cdc42 inhibition, including CASIN/CASin-related pharmacological approaches, applied to cellular aging and stem cell rejuvenation.
Seed-backed company developing pharmacological approaches to rejuvenate aged hematopoietic stem cells.
Supplied evidence states Mogling Bio targets Cdc42 overactivation to rejuvenate aged and exhausted cells and restore stem cell function.
Cdc42 multiple myeloma drug resistance program
preclinicaldrug program · medium
Overcome drug resistance in multiple myeloma by targeting Cdc42.
Rational targeting of Cdc42 in multiple myeloma models.
Preclinical publication listed for Cdc42 targeting in multiple myeloma drug resistance.
Publication title states rational targeting of Cdc42 overcomes drug resistance of multiple myeloma.
Cdc42/NK cell immune dysfunction program
exploratoryresearch program · medium
Understand and potentially restore impaired cytotoxic function of NK cells from older individuals against senescent fibroblasts.
Research on Cdc42 GTPase overactivation in NK cells from old individuals and its effect on cytotoxic function.
Publication listed on Cdc42 overactivation impairing NK cell cytotoxicity in old individuals.
Publication title indicates Cdc42 GTPase overactivation impairs cytotoxic function of NK cells from old individuals toward senescent fibroblasts.
Cdc42 regulatory T-cell antitumor immunity program
preclinicalresearch program · medium
Enhance antitumor T-cell immunity by targeting Cdc42 GTPase in regulatory T cells.
Cdc42 GTPase targeting in regulatory T cells.
Preclinical publication listed on Cdc42 targeting in regulatory T cells and antitumor immunity.
Publication title states targeting Cdc42 GTPase in regulatory T cells unleashes antitumor T-cell immunity.
CDC42-targeted hematologic malignancy drug-resistance program
preclinicalresearch program · medium
Overcome drug resistance or chemoresistance in hematologic cancers by targeting CDC42-related mechanisms.
CDC42 targeting and quinacrine-CASIN combination approaches in multiple myeloma and human acute lymphoid leukemia research contexts.
Mogling Bio listed publications titled “Rational Targeting of Cdc42 Overcomes Drug Resistance of Multiple Myeloma” and “Quinacrine-CASIN combination overcomes chemoresistance in human acute lymphoid leukemia.”
Publication titles report overcoming drug resistance in multiple myeloma through CDC42 targeting and overcoming chemoresistance in human acute lymphoid leukemia with a quinacrine-CASIN combination.
Cdc42 targeting for multiple myeloma drug resistance
preclinicaldrug program · medium
Overcome drug resistance in multiple myeloma by rationally targeting Cdc42.
Cdc42-targeted therapeutic approach in multiple myeloma drug-resistance research.
Mogling Bio lists a publication titled “Rational Targeting of Cdc42 Overcomes Drug Resistance of Multiple Myeloma.”
The listed publication title reports that rational targeting of Cdc42 overcomes drug resistance of multiple myeloma.
Cdc42 targeting in regulatory T cells for antitumor immunity
preclinicalresearch program · medium
Enhance antitumor T-cell immunity by targeting Cdc42 GTPase in regulatory T cells.
Cdc42 GTPase targeting in regulatory T cells.
Mogling Bio lists a publication titled “Targeting of Cdc42 GTPase in regulatory T cells unleashes antitumor T-cell immunity.”
The listed publication title reports that targeting Cdc42 GTPase in regulatory T cells unleashes antitumor T-cell immunity.
Non-myeloablative hematopoietic stem cell engraftment approach
preclinicalresearch program · medium
Enable long-term engraftment of human and mouse hematopoietic stem cells without myeloablative conditioning.
Non-myeloablative conditioning approach for hematopoietic stem cell engraftment.
Mogling Bio lists a publication titled “A non-myeloablative conditioning approach for long-term engraftment of human and mouse hematopoietic stem cells.”
The listed publication title reports a non-myeloablative conditioning approach for long-term engraftment of human and mouse hematopoietic stem cells.
Non-myeloablative hematopoietic stem cell engraftment program
preclinicalresearch program · medium
Enable long-term engraftment of human and mouse hematopoietic stem cells using a non-myeloablative conditioning approach.
Non-myeloablative conditioning method for hematopoietic stem cell engraftment in human and mouse contexts.
Mogling Bio listed the publication “A non-myeloablative conditioning approach for long-term engraftment of human and mouse hematopoietic stem cells.”
The publication title reports long-term engraftment of human and mouse hematopoietic stem cells using a non-myeloablative conditioning approach.
Quinacrine-CASIN acute lymphoid leukemia chemoresistance program
preclinicaldrug program · medium
Overcome chemoresistance in human acute lymphoid leukemia.
Combination treatment using quinacrine and CASIN.
Preclinical publication listed for quinacrine-CASIN combination in human acute lymphoid leukemia.
Publication title states the quinacrine-CASIN combination overcomes chemoresistance in human acute lymphoid leukemia.
Quinacrine-CASIN combination for acute lymphoid leukemia chemoresistance
preclinicaldrug program · medium
Overcome chemoresistance in human acute lymphoid leukemia.
Combination treatment using quinacrine and CASIN.
Mogling Bio lists a publication titled “Quinacrine-CASIN combination overcomes chemoresistance in human acute lymphoid leukemia.”
The listed publication title reports that the quinacrine-CASIN combination overcomes chemoresistance in human acute lymphoid leukemia.
