Key Patents Granted For Probiodrug AG’s pGlu-Abeta Targeting Monoclonal Antibody Program For The Treatment Of Alzheimer’s Disease
HALLE/SAALE, Germany, 11 January 2016 – Probiodrug AG (Euronext Amsterdam: PBD), a biopharmaceutical company developing novel therapeutic solutions to treat Alzheimer’s disease (AD), announces, that key patents for its antibody program targeting pyroglutamate Abeta (pGlu-Abeta, also N3pG Abeta), were granted during the last quarter of 2015. Patents US 9,156,907 and JP 5,828,762, were granted in the US and in Japan, respectively, covering method as well as composition of matter claims.
A variant of amyloid beta, pGlu-Abeta has been shown to form hyper-neurotoxic Abeta-Oligomers, which are supposed to be a key component leading to neurodegeneration and cognitive impairment. Probiodrug focuses on two pGlu-Abeta targeting approaches for the treatment of AD:
(i) PQ912, a small molecule inhibitor of Glutaminyl Cyclase, which prevents pGlu-Abeta formation and is currently in a Phase II trial.
(ii) PBD-C06, a monoclonal antibody, binding specifically to pGlu-Abeta, is currently in preclinical development. The company has validated the concept of targeting pGlu-Abeta by both means in preclinical studies and published data in a number of publications1,2.
While PQ912 is first in class, the pGlu-specific antibody PBD-C06 follows the monoclonal antibody LY3002813 developed by Eli Lilly, which has been advanced into a Phase Ib study in AD patients3. In this context, LY3002813, in addition to having an effect as a mono-therapy in an AD mouse model, also revealed an additive/synergistic effect on brain levels of Abeta when combined with a BACE inhibitor4.
Konrad Glund, CEO of Probiodrug, commented: “The patents granted by the US and Japanese patent offices are important milestones that strengthen our position in the development of an immunotherapy for AD based on a pGlu-Abeta specific monoclonal antibody. Probiodrug’s strategy to tackle pGlu-Abeta with two complementary approaches offers the ability to study the efficacy of each respective single agent, as well as in combination with each other, and with products that have different mode of action to treat AD.”
1Frost et al., Neurobiology of Aging 36 (2015) 3187-3199; 2Frost et al., The American Journal of Pathology, Vol. 183, No.
2, August 2013; 3clinicaltrials.gov, January 11th 2016; 4DeMattos et al., Alzheimer’s & Dementia (2015) Vol.11, Issue 7, Supplement, Pages P275–P276
A variant of amyloid beta, pGlu-Abeta has been shown to form hyper-neurotoxic Abeta-Oligomers, which are supposed to be a key component leading to neurodegeneration and cognitive impairment. Probiodrug focuses on two pGlu-Abeta targeting approaches for the treatment of AD:
(i) PQ912, a small molecule inhibitor of Glutaminyl Cyclase, which prevents pGlu-Abeta formation and is currently in a Phase II trial.
(ii) PBD-C06, a monoclonal antibody, binding specifically to pGlu-Abeta, is currently in preclinical development. The company has validated the concept of targeting pGlu-Abeta by both means in preclinical studies and published data in a number of publications1,2.
While PQ912 is first in class, the pGlu-specific antibody PBD-C06 follows the monoclonal antibody LY3002813 developed by Eli Lilly, which has been advanced into a Phase Ib study in AD patients3. In this context, LY3002813, in addition to having an effect as a mono-therapy in an AD mouse model, also revealed an additive/synergistic effect on brain levels of Abeta when combined with a BACE inhibitor4.
Konrad Glund, CEO of Probiodrug, commented: “The patents granted by the US and Japanese patent offices are important milestones that strengthen our position in the development of an immunotherapy for AD based on a pGlu-Abeta specific monoclonal antibody. Probiodrug’s strategy to tackle pGlu-Abeta with two complementary approaches offers the ability to study the efficacy of each respective single agent, as well as in combination with each other, and with products that have different mode of action to treat AD.”
1Frost et al., Neurobiology of Aging 36 (2015) 3187-3199; 2Frost et al., The American Journal of Pathology, Vol. 183, No.
2, August 2013; 3clinicaltrials.gov, January 11th 2016; 4DeMattos et al., Alzheimer’s & Dementia (2015) Vol.11, Issue 7, Supplement, Pages P275–P276