Immungenetics AG, a German based biopharmaceutical company focusing on novel treatments for unmet medical needs in the field of neurodegenerative, autoimmune diseases and aging, announced today that the last study visit of the last patient enrolled (Last Patient’s Last Visit, LPLV) occurred on 06 June 2018 in the first subgroup of DrainAD, a Phase II proof-of-concept study for the early diagnosis and causative therapy of Alzheimer’s Disease (AD).
The DrainAD study is structured in two parts aiming at the early detection and monitoring of AD by means of a blood test, as well as at developing a novel treatment for altering the course of the disease; a treatment that may halt or even reverse disease progression.
The completed subgroup of fourteen participants (seven patients with newly diagnosed early-to-mild dementia due to Alzheimer’s Disease and seven healthy volunteers) received a daily dosage of 26 mg of the drug thiethylperazine for four consecutive days. The investigation was conducted at the University of Göttingen under supervision of Prof. Jens Wiltfang. More than 150 blood samples were obtained and will be analyzed at five labs under different aspects.
Interim results for the primary endpoints safety and tolerability as well as efflux of amyloid beta peptides after drug administration are expected to be available in the third quarter of 2018. These findings will also serve to decide if a similar exercise with a 52 mg daily regimen is to be undertaken. Additional data mining will deliver further insights later this year.
"This is a significant milestone towards elucidating this novel angle of attack against this devastating disease.", commented Antonio Martinez Arbizu, CEO of Immungenetics. "We would like to thank all trial participants and medical professionals who helped executing step one of DrainAD, and are very much looking forward to share our results in a couple of months."
The new mechanism of action being investigated by DrainAD is the capability of thiethylperazine to activate so called ABC-transporters,  especially ABCC1 at the chosen dosage. ABC-transporters located at the blood-brain barrier are in charge of the export of toxic substances like beta amyloid species (ABeta) from the brain into the blood stream. This was demonstrated by Prof. Jens Pahnke (University of Rostock then, now University of Oslo) in transgenic AD-mice: treated with thiethylperazine, toxic ABeta was reduced by 70% within 25 days (1).
In a second, award winning research paper, Pahnke proved the ABC transporter hypothesis in a non-transgenic early AD mouse model. The article verified recent evidence that sporadic Alzheimer’s disease (AD), which counts for more than 98% of all cases, is not caused by an overproduction of the neurotoxic ABeta peptide but by its impaired clearance from the brain and that soluble ABeta species are the main scourge of the disease (2).

Science:
1) Krohn et al. 2011: "Cerebral amyloid-β proteostasis is regulated by the membrane transport protein ABCC1 in mice." J Clin Invest. 2011 Oct 3; 121(10): 3924-3931.
2) Krohn et al. 2015: "Accumulation of murine amyloid-β mimics early Alzheimer’s disease." Brain, 138(Pt8):2370-82.