Hemostemix’s patented ACP-01 and NCP-01 autologous cell therapies demonstrate potential to extend brain–computer interface functional lifespan beyond one year by modulating inflammatory responses, stimulating angiogenesis through VEGF and IL-8 signaling, and enhancing synaptogenesis and neural plasticity. This approach aims to improve implant integration and signal fidelity for advanced neuroprosthetic applications.
Key points
- ACP-01 secretes CXCL8, VEGF, and angiogenin to recruit NK cells and CD34+ progenitors, driving angiogenesis and inflammation suppression at BCI sites.
- NCP-01 utilizes CXCR4-mediated homing to implant regions, differentiates into neuronal and glial cells, and supports synaptogenesis for improved signal integration.
- Combined intracerebrospinal delivery of ACP-01 and NCP-01 addresses inflammatory scarring and neural loss, potentially extending BCI functional lifespan and maintaining signal fidelity.
Why it matters: This dual-cell approach could transform neuroprosthetic interfaces by significantly extending implant longevity, enhancing signal quality, and improving patient outcomes.
Q&A
- What are ACP-01 and NCP-01 precursors?
- How does ACP-01 promote angiogenesis around implants?
- Why is inflammation reduction critical for BCI durability?
- What role does NCP-01 play in neural integration?