ProMIS offeri potential significant advantage over aducanumab, learns from mistakes

ProMIS Neurosciencesissued a pres release Thursday, raising the question of urgency to selectively target the toxic oligomer with exacting precision as part of the global effort to develop disease-modifying therapies for Alzheimer’s disease (AD), upon Biogen’s and Eisai’s dropping two alte-stage clinical trials of aducanumab.

As it said, on March 20, Biogen and its partner, Eisai, terminated two late-stage clinical trials of aducanumab, which could have offered a disease-modifying therapy for Alzheimer’s disease.

Promis said last yeari t could bring the competition to Biogen’s candidate in aducanumab, noting it’s lead product candidate for Alzheimer’s disease, PMN310, showed similar ability to cross the blood brain barrier and penetrate the central nervous system (CNS) compared to Biogen’s aducanumab.

Promis Thursday noted that the termination of aducanumab phase 3 trials, along with the discontinuation of the crenezumab program by Roche Holdings and partner AC Immune announced on January 30, underscores the urgent need for drug candidates that are highly selective for the toxic oligomer form of amyloid beta (Aβ). Aducanumab was not selective enough as it binds mainly to the plaque form of Aβ. Likewise, crenezumab was not selective for the toxic oligomer as it binds all forms of Aβ, ProMIS said.

Dr. James Kupiec, ProMIS Chief Medical Officer, said: “These are the hard lessons of science, but there’s hope. Aducanumab was developed over a decade ago to go after plaque, which we have since learned is the incorrect therapeutic target because plaque is a largely non-toxic form of amyloid beta.”

Furthermore, he said that aducanumab wasted too much limited ammunition on the wrong target, which also led to the dose limiting side effect of brain swelling (edema).

He explained that, unlike aducanumab, ProMIS’ lead antibody candidate for Alzheimer’s, PMN310, reflects key lessons learned, namely that the toxic oligomer of amyloid beta is a root cause of AD, not plaque.

“PMN310 is the first antibody to selectively target just the toxic oligomer, a misfolded, toxic form of amyloid beta, offering a potential significant advantage over aducanumab and other less selective antibodies in terms of both efficacy and safety,” he said.