J&J backs Prazer’s ₩29 bil. raise as startup targets a 2026 tech transfer in Alzheimer’s

Korea-based biotech Prazer Therapeutics says it can move targeted protein degradation (TPD) into the brain, a step the field has struggled to achieve because of the blood-brain barrier and uneven ligase expression.

After raising 29 billion won ($21 million) Series B in April led by Johnson & Johnson’s venture arm JJDC, with new investors Premier Partners, K2 Investment, Mirae Asset Capital, Quad Asset Management and STIC Ventures and follow-on investments from Company K Partners, Kiwoom Investment and Smilegate Investment, the Seoul startup is preparing a global out-license by late 2025 to early 2026.

The company remains a JLABS member and plans to use the funding to expand its pipeline and global business development.

Prazer’s platform, SPiDEM, aims for a more flexible degrader design. Instead of tying each drug to a single recruited E3 ligase, the tagging enzyme, and to the proteasome, the cell’s protein recycler, SPiDEM compounds induce ubiquitination through the E3 that naturally associates with the target and then route the protein to either the proteasome or the lysosome for clearance, depending on the biology.

In an interview with Korea Biomedical Review, CEO Inn Kyung-soo called SPiDEM “a new key” for targets that classic PROTACs and molecular glues, two dominant TPD formats, have struggled to reach, including membrane proteins and protein aggregates. 

The first disease area is neurodegeneration. Prazer is focusing on Alzheimer’s, with tau and α-synuclein programs, arguing that SPiDEM’s use of lysosomal and autophagy pathways, the cell’s clearance systems, could matter where toxic aggregates drive the disease.

The company declined to provide investigational new drug (IND) application timing while partnership talks are active, but the near-term objective is explicit: complete a technology-transfer with a global pharmaceutical company by late 2025 to the first half of 2026.

Prazer’s collaboration with Yuhan Corp., signed in July 2024, lays out a two-stage plan on an undisclosed target. Stage one targets hit identification: Prazer leads synthesis and primary screens; Yuhan runs in-vitro evaluation. Stage two aims for candidate selection: Prazer conducts optimized synthesis and primary screening; Yuhan leads in-vitro and in-vivo efficacy, DMPK and non-GLP toxicology. Yuhan pays fixed research fees as work progresses. 

Program outputs are jointly owned 50/50, while Prazer retains sole ownership of SPiDEM core know-how, including its ubiquitin-recruiting moiety (URM) intellectual property. The data are “too early to disclose,” Inn said, adding that work is proceeding to plan.

The company’s recent financing continues a string of external validations. Prazer won the 2022 Seoul-BMS Innovation Challenge and took second place in Boehringer Ingelheim Japan’s 2023 innovation awards.

In a 2024 Seoul Economic Daily interview, Inn described the BMS challenge as a year-long, hands-on mentorship that “objectively validated” the platform and sharpened its approach to big-pharma dialogues -- support that Prazer credits with improving its business development readiness.

Beyond Yuhan, Prazer confirmed joint research with Korea’s Daewon Pharmaceutical and said discussions with multiple global pharmas are under way, especially in neurodegeneration where scale and clinical infrastructure are decisive. 

The competitive context continues to shift. Arvinas’ ARV-102 data indicate that brain-penetrant degraders are achievable, while Kymera, after signing an option-to-license agreement with Gilead for CDK2 molecular glues, has reported early human signals with its STAT6 degrader, KT-621, in inflammatory disease. Together, these moves broaden TPD beyond oncology and show the modality’s reach. 

Reviews over the past year have also cataloged the central hurdles for CNS TPD -- molecular size, polarity and delivery -- and the strategies to address them, underscoring why a blood-brain-barrier-capable platform would be notable if Prazer can produce preclinical evidence in disease-relevant models.