"Because FcRn also regulates Ab half-life, Fc mutations like the M428L/N434S, commonly known as LS mutations, and others have been developed to enhance binding affinity to FcRn and improve drug pharmacokinetics."

" We also generated a stabilized and FcRn-enhanced form of leronlimab,"

Q: created our own mutation, that binds to FcRn, for delivering Leronlimab?

" Leronlimab-PLS maintained higher levels within the maternal compartment while also reaching higher mAb levels in the fetus and newborn circulation."

Q: Higher than the drug M428L & N434S delivers?

"Further, a single dose of leronlimab-PLS led to complete CCR5 receptor occupancy in mothers and newborns for almost a month after birth"

Q: No LL SAE's reported.

Finding out what drug(s) M428L & N434S delivers, is needed for SAE look.
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The neonatal Fc receptor (FcRn) is a receptor that can bind to several types of viruses, including echoviruses and arteriviruses:

Echoviruses
FcRn is a receptor for echoviruses, which are a common cause of aseptic meningitis in neonates and young children. Echoviruses can cause severe disease, including hepatitis, neurological disease, and death. FcRn is expressed in the placenta, intestines, liver, and blood-brain barrier, which are the primary and secondary sites of infection for echoviruses.

Arteriviruses
FcRn is a receptor for arteriviruses, which are enveloped viruses that can cause a variety of diseases, including pneumonia, encephalitis, and hemorrhagic fever. FcRn is required for arteriviruses to enter cells, and it works with CD163, another arterivirus entry factor. Anti-FcRn antibodies can block arterivirus infection

Q: So being LL is a large Mab molecule, is it binding harder to FcRn, blocking viruses / disease, via the placenta?

Same as to what LL does to Rantes?

So far outstanding what they've reported in the publication.

& no cost to Cytodyn.