Early Intervention to Limit Alzheimer’s Disease
Pipeline
Praetego is currently developing Amadorin candidate PTG-630 as an early intervention to limit Alzheimer’s disease.
Alzheimer’s Disease (AD)
Alzheimer’s disease imparts a tremendous burden on patients, caregivers, and our healthcare system. Rather than treating the disease after overt cognitive deficits are present, we need an early intervention. In multiple long-term transgenic animal models of AD, PTG-630 protects memory, reverses cognitive decline once present, and demonstrates other neuroprotective features. Intended as an oral candidate, it is highly absorbed, crosses the blood-brain barrier, and permeates brain tissue.
This work is funded in part by the National Institute of Aging (NIA) of the NIH.
Diabetic Peripheral Neuropathy (DPN)
Diabetic Peripheral Neuropathy (DPN)—a degenerative process of the nerves, typically starts in the extremities. Affecting approximately 50% of diabetics, DPN can be very painful and debilitating. It can also lead to an increase fall risk, foot ulcers and amputations.
In long-term animal models of DPN, treatment with PTG-630 restored nerve function. It reversed nerve deficits in both large and small nerve fibers. PTG-630 is demonstrating neuroprotective and neurorestorative effects in the animal model of DPN.
This work is funded in part by the National Institute of Diabetic and Digestive and Kidney Diseases (NIDDK) of the NIH.
Diabetic Retinopathy (DR)
Diabetic Retinopathy is a leading cause of blindness. Starting as a neurovascular degenerative process, DR leads to vascular damage to the retina and loss of vision. The retina serves as a critical connection of visual data and neural processing. Current treatments for DR include intravitreal injections to inhibit further vascular damage. While these eye injections are moderately effective, they are initiated after substantial irreversible damage has occurred. As oral candidates, the Amadorins are designed to be initiated prior to significant retinal compromise, thus preserving visual function. Preliminary data suggest PTG-630 will be a valuable oral agent against DR.
This work is funded in part by the National Eye Institute (NEI) of the NIH.
Lead Candidate
PTG-630
From our nonclinical work, PTG-630 is demonstrating a wide therapeutic window and minimal risk of drug-drug interactions. With good bioavailability, PTG-630 is well distributed in tissue. It easily crosses the Blood Brain Barrier (BBB). In animal efficacy studies, PTG-630 has consistently demonstrated protection of both the Central Nervous System (CNS) and the Peripheral Nervous System (PNS) in rodent models of Alzheimer’s Diseases and Diabetic Peripheral Neuropathy. The data demonstrates functional benefits in both models that have been confirmed by direct biochemical measures of neurodegeneration.
Amadorins: Clinical Proof of Mechanism Lead to Refinement over Multiple Generations
The Amadorins have been developed and tested over 4 generations. The original Amadorin demonstrated clinical efficacy against Diabetic Kidney Disease.
Novel candidates under development (PTG-630 and PTG-670) offer the greatest potency and margin of safety in nonclinical testing. The Amadorins are protected by an issued patent (3rd gen) and patent protection pending for the class of candidates under development (4th gen).