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$ANNX was founded on Ben Barres discovery that C1q prunes synapses in normal development and neurodegen. ANNX ultimate aim, I think, is Alzheimers, but more efficient paths first in Guillain-Barre Syndrome (GBS), Huntington's, and ALS.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742932/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742932/
GBS basics:
-Neuropathy
-Triggered by infection
-Awful acute phase lasts weeks to months followed by years long recovery and often permanent damage.
-12,000/year NA/Europe
$ANNX single dose-finding ph1b showed nice dose response, NfL reduction, and target inhibition.
-Neuropathy
-Triggered by infection
-Awful acute phase lasts weeks to months followed by years long recovery and often permanent damage.
-12,000/year NA/Europe
$ANNX single dose-finding ph1b showed nice dose response, NfL reduction, and target inhibition.
$ANNX's GBS (highest probability indication) pivotal reads in 2023.
n=~24 ph2 studies in HD and ALS will read in 2H21.
$370m cash, $1.1b cap. Low burn.
n=~24 ph2 studies in HD and ALS will read in 2H21.
$370m cash, $1.1b cap. Low burn.
Competitively, $ANNX is first to the clinic with C1q inhibitor.
vs. other complement targets, C1q looks most promising where complement is attacking neural synapses in periphery or CNS. C1q sees bound antibodies and initiates classical complement cascade.
vs. other complement targets, C1q looks most promising where complement is attacking neural synapses in periphery or CNS. C1q sees bound antibodies and initiates classical complement cascade.
Big picture, we already know that complement inhibition can rescue red blood cells, nephrons, retinas, and probably inflamed blood vessels. $ANNX is the purest play on the bet that synapses are next.
