GBA Therapeutics

This page collects therapeutic strategies from the GBA-PD pilot range. It is a source-cited map, not a final interpretation.

Strategy Map

strategycorpus representationsources
IsofagomineAppears in the summary area before eliglustat.20240722_181748
EliglustatCovered through GD type 1 trial material and continuation into the next photo.Eliglustat
AmbroxolCovered by mechanism, preclinical evidence, and clinical-trial sections.Ambroxol
Venglustat / ibiglustatCovered by preclinical, in-house, biomarker, MOVES-PD, and clinical-trial sections.Venglustat
PR001 / LY3884961Covered by preclinical mouse models, NHP ICM biodistribution, GCase activity/expression, lipid accumulation, insoluble alpha-synuclein, dose selection, and clinical-trial entry.PR001

Pilot Comparison

programprimary therapeutic idea in pilotpilot caveat
EliglustatGCS inhibition in GD1, with marketed oral GD1 context and trials such as ENCORE, ENGAGE, EDGE, and earlier P2/P1 work.Pilot pages are GD-heavy; PD relevance is marked uncertain or ? in the source summary.
AmbroxolPharmacological chaperone / GBA activator logic, including mutant-GCase folding and lysosomal delivery.Source notes explicitly state null mutations may not benefit.
VenglustatGCS inhibition; lipid lowering in GD/GBA-PD contexts and MOVES-PD.MOVES-PD clinical outcome did not separate from placebo on MDS-UPDRS II+III in the cited 52-week result.
PR001AAV/GBA gene therapy aiming to raise GCase and influence downstream lipids/alpha-synuclein.Source pages contain multiple dose bases and several high-risk vector-genome numeric values that need careful preservation.

PR001 Notes

The seed PR001 evidence emphasizes whether gene therapy changes GCase activity/expression and downstream disease-relevant readouts. The corpus includes mouse genetic model data, A53T + CBE model material, NHP biodistribution, and dose-selection text. Sources: 20240722_181805, 20240722_181809.

Next Entity Pages

  • entities/compounds/isofagomine.md after more source evidence appears.