
ADS024:
An LPAR3-targeted
biotherapeutic

ADS024:
An LPAR3-targeted
biotherapeutic

ADS024:
An LPAR3-targeted
biotherapeutic

ADS024:
An LPAR3-targeted
biotherapeutic
ADS024 is a non engrafting, naturally occurring single strain live biotherapeutic product (SS-LBP).
It is an orally dosed, anti-inflammatory SS-LBP that produces a selective agonist of the G protein-coupled receptor (GPCR) Lysophosphatidic acid receptor 3 (LPAR3).
ADS024 is a non engrafting, naturally occurring single strain live biotherapeutic product (SS-LBP).
It is an orally dosed, anti-inflammatory SS-LBP that produces a selective agonist of the G protein-coupled receptor (GPCR) Lysophosphatidic acid receptor 3 (LPAR3).
THE TARGET, LYSOPHOSPHATIDIC ACID RECEPTOR 3 (LPAR3)
THE TARGET, LYSOPHOSPHATIDIC ACID RECEPTOR 3 (LPAR3)
THE TARGET, LYSOPHOSPHATIDIC ACID RECEPTOR 3 (LPAR3)
LPAR3 is a G-protein coupled receptor (GPCR) in the EDG family of receptors (S1PRs/LPARs) known to modulate inflammation.
LPAR3 is expressed in the brain and has genetic associations with biomarkers in Alzheimer’s Disease.
LPAR3 agonism is a novel disease-modifying approach to neurodegeneration.
LPAR3 is a G-protein coupled receptor (GPCR) in the EDG family of receptors (S1PRs/LPARs) known to modulate inflammation.
LPAR3 is expressed in the brain and has genetic associations with biomarkers in Alzheimer’s Disease.
LPAR3 agonism is a novel disease-modifying approach to neurodegeneration.
LPAR3 is a G-protein coupled receptor (GPCR) in the EDG family of receptors (S1PRs/LPARs) known to modulate inflammation.
LPAR3 is expressed in the brain and has genetic associations with biomarkers in Alzheimer’s Disease.
LPAR3 agonism is a novel disease-modifying approach to neurodegeneration.





POTENT AGONISM
ADS024 is cultured to produce a potent selective agonist of LPAR3.
The bacteria is then lyophilized to a powder form that can be dosed orally.
GI RELEASE
The LPAR3 agonist remains
stably associated with ADS024 until it is orally dosed.
Studies in mice show that > 99.9% of the bacteria do not survive transit through the stomach and small intestine, therefore the LPAR3 agonist is likely released in the upper GI tract.
BRAIN EFFICACY
ADS024 has shown efficacy
in an AD model and in multiple models of other neurodegenerative and neuroinflammatory diseases suggesting impact regardless of the cause of damage.
The preclinical dataset generated to date strongly supports moving into human testing in AD patients.
POTENT AGONISM
POTENT AGONISM
ADS024 is cultured to produce a potent selective agonist of LPAR3.
The bacteria is then lyophilized to a powder form that can be dosed orally.
ADS024 is cultured to produce a potent selective agonist of LPAR3.
The bacteria is then lyophilized to a powder form that can be dosed orally.
GI RELEASE
GI RELEASE
The LPAR3 agonist remains
stably associated with ADS024 until it is orally dosed.
Studies in mice show that > 99.9% of the bacteria do not survive transit through the stomach and small intestine, therefore the LPAR3 agonist is likely released in the upper GI tract.
The LPAR3 agonist remains
stably associated with ADS024 until it is orally dosed.
Studies in mice show that > 99.9% of the bacteria do not survive transit through the stomach and small intestine, therefore the LPAR3 agonist is likely released in the upper GI tract.
BRAIN EFFICACY
BRAIN EFFICACY
ADS024 has shown efficacy
in an AD model and in multiple models of other neurodegenerative and neuroinflammatory diseases suggesting impact regardless of the cause of damage.
The preclinical dataset generated to date strongly supports moving into human testing in AD patients.
ADS024 has shown efficacy
in an AD model and in multiple models of other neurodegenerative and neuroinflammatory diseases suggesting impact regardless of the cause of damage.
The preclinical dataset generated to date strongly supports moving into human testing in AD patients.