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Recent Comments
Congratulations to you and the team on this fantastic work! đź‘Ź
Designing a retroviral tricistronic vector to simultaneously tackle three distinct axes of immune evasion converting PD-L1 into an activating signal, blocking HLA-E/NKG2A, and incorporating autocrine IL-15 is a remarkably elegant approach to arming "off-the-shelf" NK cells against a hostile TME.
Given the long-term persistence observed after a single administration, I am particularly curious about the safety and regulation profile: Do you anticipate any potential for autonomous/uncontrolled NK cell expansion or systemic toxicity driven by the continuous low-level IL-15 secretion, or does the local autocrine loop keep cytokine activity tightly localized to the tumor site?
Exciting progress for cell therapy looking forward to seeing how this platform advances toward clinical trials!
Your development story beautifully proves that tracking total active plasma concentration can mask crucial tissue specific liabilities. By isolating the higher brain penetration and GABA-A potency of the M2 metabolite, you successfully decoupled systemic oncological efficacy from CNS toxicity.
Does this deuteration induced metabolic shift toward lower M2 levels also mitigate the strong hepatic CYP induction and drug-drug interaction profile seen historically with enzalutamide?
Thank you for the detailed and clear explanation, Dr. Xinghai! It's fantastic to see how the deuteration-driven metabolic shift cleanly addresses both the CNS liabilities and the CYP-mediated DDI challenges.
I would love to take a look at the underlying PK data and comparative profiles if you are open to sharing. Thanks again for the great insights!
Your development story beautifully proves that tracking total active plasma concentration can mask crucial tissue specific liabilities. By isolating the higher brain penetration and GABA-A potency of the M2 metabolite, you successfully decoupled systemic oncological efficacy from CNS toxicity.
Does this deuteration induced metabolic shift toward lower M2 levels also mitigate the strong hepatic CYP induction and drug-drug interaction profile seen historically with enzalutamide?