"Revolution Medicines is developing a portfolio of oral "RAS(ON)" inhibitors targeting various KRAS mutations (G12C, G12D, G12V, G13C, Q61H) by binding to the active state of the protein. Key candidates include zoldonrasib (RMC-9805) for G12D, elironrasib (RMC-6291) for G12C, and daraxonrasib (RMC-6236), a pan-RAS inhibitor, all showing promise in early clinical trials for lung and pancreatic cancers.
Key Revolution Medicine KRAS Candidates:
Zoldonrasib (RMC-9805 - KRAS G12D): Received FDA Breakthrough Therapy Designation for previously treated KRAS G12D-mutated metastatic NSCLC, with trials showing high disease control rates"
Revolution is up like 30 bucks earlier today
"Yes, KRAS-mutant tumors often express CCR5 (C-C motif chemokine receptor-5) and its ligand, CCL5. The activation of the KRAS pathway, particularly in colorectal and pancreatic cancers, is associated with the remodeling of the tumor microenvironment (TME) to promote an inflammatory, pro-tumorigenic environment that includes the overexpression of CCR5.
Here are the key details regarding KRAS mutations and CCR5 expression:
Immune Cell Recruitment: CCR5 is typically expressed on T cells, macrophages, and dendritic cells. In KRAS-mutant cancers (like colorectal cancer), high levels of CCR5 are involved in recruiting these inflammatory cells to the tumor site.
Oncogenic Transformation: The expression of CCR5 can be induced by oncogenic transformations (such as Ras mutations).
CCL5/CCR5 Axis: KRAS mutations promote the secretion of CCL5 (the ligand for CCR5), which helps activate CCR5 signaling, supporting cancer cell survival, invasion, and metastasis"
Thanks!! SC
Key Revolution Medicine KRAS Candidates:
Zoldonrasib (RMC-9805 - KRAS G12D): Received FDA Breakthrough Therapy Designation for previously treated KRAS G12D-mutated metastatic NSCLC, with trials showing high disease control rates"
Revolution is up like 30 bucks earlier today
"Yes, KRAS-mutant tumors often express CCR5 (C-C motif chemokine receptor-5) and its ligand, CCL5. The activation of the KRAS pathway, particularly in colorectal and pancreatic cancers, is associated with the remodeling of the tumor microenvironment (TME) to promote an inflammatory, pro-tumorigenic environment that includes the overexpression of CCR5.
Here are the key details regarding KRAS mutations and CCR5 expression:
Immune Cell Recruitment: CCR5 is typically expressed on T cells, macrophages, and dendritic cells. In KRAS-mutant cancers (like colorectal cancer), high levels of CCR5 are involved in recruiting these inflammatory cells to the tumor site.
Oncogenic Transformation: The expression of CCR5 can be induced by oncogenic transformations (such as Ras mutations).
CCL5/CCR5 Axis: KRAS mutations promote the secretion of CCL5 (the ligand for CCR5), which helps activate CCR5 signaling, supporting cancer cell survival, invasion, and metastasis"
Thanks!! SC
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