SciNeuro and Novartis sign $1.7 billion Alzheimer's drug deal

Chinese biotech firm SciNeuro Pharmaceuticals has partnered with Swiss pharmaceutical giant Novartis in a deal worth nearly $1.7 billion to develop treatments for Alzheimer's disease, which affects some 55 million people worldwide. The agreement grants Novartis exclusive worldwide rights to develop and commercialise SciNeuro's antibody candidates for the progressive brain disease. SciNeuro's novel amyloid beta-targeted antibody programme leverages proprietary blood-brain barrier shuttle technology to help more of the drug cross into the brain where Alzheimer's damage occurs.

On Monday, China's SciNeuro Pharmaceuticals announced a partnership with Swiss pharmaceutical giant Novartis, reviving hopes for treating Alzheimer's disease, which affects some 55 million people worldwide and could cost the global economy $2.8 trillion by 2030.

The deal, valued at nearly $1.7 billion, grants Novartis exclusive worldwide rights to develop and commercialise SciNeuro's antibody candidates for drugs targeting the progressive brain disease. SciNeuro's novel amyloid beta-targeted antibody programme is one of the firm's key strategic research and development priorities and leverages proprietary blood-brain barrier shuttle technology to enable more of the drug to cross into the brain where Alzheimer's damage occurs.

"The anti-amyloid programme represents one of SciNeuro's key strategic research and development priorities to target the neurodegenerative disease," said Li Min, founder and CEO of SciNeuro. "This collaboration delivers an optimal synergy, combining our expertise in disease biology and early development with Novartis' global leadership in clinical development and commercialisation."

Under the agreement, SciNeuro will receive an upfront payment of $165 million and could earn up to $1.5 billion in development, regulatory, and commercial milestones, plus royalties on future sales.

Over the past three decades, amyloid beta protein has been a primary drug target for the treatment and prevention of Alzheimer's disease. This approach has been backed by extensive laboratory and genetic evidence from scientists, according to a 2023 review on amyloid-based therapy published in a Nature-affiliated journal.

The partnership highlights the growing role of Chinese biotech firms in global pharmaceuticals and may accelerate progress in Alzheimer's treatments, despite long-standing challenges in the field.

ተያያዥ ጽሁፎች

Illustration of a Brazilian researcher in a lab examining a rat, with screens showing brain scans and molecular structures, representing a new compound that reverses Alzheimer's-like deficits in rats.
በ AI የተሰራ ምስል

Brazilian copper-targeting compound reverses Alzheimer’s-like deficits in rats

በAI የተዘገበ በ AI የተሰራ ምስል እውነት ተፈትሸ

Researchers at Brazil’s Federal University of ABC report a simple copper-chelating molecule that reduced beta-amyloid–linked pathology and improved memory in rats. The compound showed no detectable toxicity in preclinical tests and, based on computer modeling, is predicted to cross the blood–brain barrier. The team is seeking industry partners for clinical development.

Alzheimer's trials are shifting to a multi-target approach inspired by cancer research, even after failures with Novo Nordisk's semaglutide. Only two drugs, Eli Lilly's Kisunla and Eisai and Biogen's Leqembi, are widely approved to slow progression. This evolution treats the brain-wasting disease as a complex system, seeking new ways to halt it amid its global impact.

በAI የተዘገበ

Scientists at Northwestern University have identified a toxic subtype of amyloid beta oligomers that triggers early Alzheimer's changes in the brain. Their experimental drug, NU-9, reduced this damage and inflammation in pre-symptomatic mice, suggesting potential for preventing the disease before symptoms appear. The findings highlight a new strategy for early intervention.

Researchers at Sweden’s Karolinska Institutet and Japan’s RIKEN Center for Brain Science report that two somatostatin receptors, SST1 and SST4, jointly regulate levels of neprilysin—an enzyme that breaks down amyloid-beta—in the hippocampus. In mouse models, activating the receptors raised neprilysin, reduced amyloid-beta buildup and improved memory-related behavior, the team said.

በAI የተዘገበ

Researchers have uncovered how amyloid beta and inflammation may both trigger synapse pruning in Alzheimer's disease through a common receptor, potentially offering new treatment avenues. The findings challenge the notion that neurons are passive in this process, showing they actively erase their own connections. Led by Stanford's Carla Shatz, the study suggests targeting this receptor could preserve memory more effectively than current amyloid-focused drugs.

Researchers at Kindai University report that oral arginine, a common amino acid, suppresses amyloid‑β aggregation and its toxic effects in fruit fly and mouse models of Alzheimer’s disease. In treated animals, amyloid buildup fell, inflammation markers dropped, and behavioral performance improved, suggesting arginine could be a low‑cost candidate for drug repurposing.

በAI የተዘገበ እውነት ተፈትሸ

New research finds that blood biomarkers associated with Alzheimer’s disease increase significantly faster in people with obesity than in those without. Drawing on five years of data from 407 volunteers, the study suggests that blood tests can detect obesity‑related changes earlier than brain scans, underscoring obesity as a major modifiable risk factor for Alzheimer’s.

 

 

 

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