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Posted On: 08/17/2025 10:42:53 PM
Post# of 265
Re: chuckles759 #248
Fair question… FDA usually waits until all custodians finish unless you ask for rolling releases. I’ve filed dozens of FOIAs already, with more lined up, so I’ll see if they play it smart or just keep digging the hole they’re in. (Unless I disappear before then… kidding
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investigations@firegatebioscience.com
Other encrypted emails available upon request.
Leronlimab (a CCR5 mAb) has very low toxicity, especially compared to most HIV drugs.
• That makes it feasible to use in higher doses (700 mg+) or in combination strategies without the safety trade-offs that normally kill “cure” attempts.
⸻
???? CCR5 Δ32 insight
• People with the CCR5 Δ32 mutation (homozygous) are famously resistant to HIV infection.
• Blocking CCR5 with a drug is essentially a therapeutic mimic of that genetic protection.
• This is why the Berlin and London “cured” patients (via stem cell transplant with Δ32 donor cells) proved the concept. Leronlimab just does it non-genetically.
⸻
???? The “hot and cold” latency angle
• PD-L1 inhibition (immune checkpoint blockade) can “wake up” latent HIV reservoirs — the so-called shock and kill approach.
• CCR5 blockade (Leronlimab) prevents new infection pathways and stabilizes immune recovery once those reservoirs are exposed.
• Combined, it’s like flipping the light switch (PD-L1 wakes hidden HIV) and then locking the doors (CCR5 blockade stops spread and allows clearance).
⸻
⚡ Why this is so dangerous for FDA/industry
It’s not exotic science. It’s brutally simple:
• Low-toxicity CCR5 blockade (Leronlimab) + latency reversal agents (PD-L1 or similar) = a functional cure path.
• The only way to make that fail is to underdose, mis-design trials, or bury combo data.
Other encrypted emails available upon request.
Leronlimab (a CCR5 mAb) has very low toxicity, especially compared to most HIV drugs.
• That makes it feasible to use in higher doses (700 mg+) or in combination strategies without the safety trade-offs that normally kill “cure” attempts.
⸻
???? CCR5 Δ32 insight
• People with the CCR5 Δ32 mutation (homozygous) are famously resistant to HIV infection.
• Blocking CCR5 with a drug is essentially a therapeutic mimic of that genetic protection.
• This is why the Berlin and London “cured” patients (via stem cell transplant with Δ32 donor cells) proved the concept. Leronlimab just does it non-genetically.
⸻
???? The “hot and cold” latency angle
• PD-L1 inhibition (immune checkpoint blockade) can “wake up” latent HIV reservoirs — the so-called shock and kill approach.
• CCR5 blockade (Leronlimab) prevents new infection pathways and stabilizes immune recovery once those reservoirs are exposed.
• Combined, it’s like flipping the light switch (PD-L1 wakes hidden HIV) and then locking the doors (CCR5 blockade stops spread and allows clearance).
⸻
⚡ Why this is so dangerous for FDA/industry
It’s not exotic science. It’s brutally simple:
• Low-toxicity CCR5 blockade (Leronlimab) + latency reversal agents (PD-L1 or similar) = a functional cure path.
• The only way to make that fail is to underdose, mis-design trials, or bury combo data.
