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Catalog Product Name CAS Number Inquiry
BP-400002 PROTAC MDM2 Degrader-3 2249750-23-8 Inquiry
BP-400017 PROTAC_ERRα Inquiry
BP-400013 CMP 98 Inquiry
BP-400025 BI-3663 Inquiry
BP-400021 SARM-nutlin PROTAC Inquiry
BP-400022 ATRA-MeBS PROTAC Inquiry
BP-400001 PROTAC AR Degrader-4 1351169-31-7 Inquiry
BP-400029 PROTAC B-Raf degrader 1 Inquiry
BP-400019 MZ 2 Inquiry
BP-400027 GMB-475 Inquiry
BP-400023 PROTAC CRBN Degrader-1 2358775-70-7 Inquiry
BP-400026 BSJ-03-123 Inquiry
BP-400007 CM 11 Inquiry
BP-400015 Protac-1 Inquiry
BP-400016 Protac-4 Inquiry
BP-400030 PROTAC ER Degrader-2 Inquiry
BP-400018 PROTAC_RIPK2 Inquiry
BP-400024 ACBI1 Inquiry
BP-400020 Compound 3i Inquiry
BP-400028 PROTAC BET degrader-3 Inquiry

PROTAC® is the abbreviation for proteolysis targeting chimera, which is a small bifunctional molecule. One end of the molecule is a ligand that binds the target protein and the other end is a ligand that binds E3 ubiquitin ligase. The two ends are connected by a chain. In vivo, the target protein and E3 ubiquitin ligase can be drawn closer, so that the target protein is labeled with ubiquitin and then degraded by the ubiquitin-proteasome pathway. This is a brand-new drug design strategy. By designing such triplet small molecule drugs, theoretically, any over-expressed and mutated pathogenic protein can be eliminated for the purpose of treating the disease.


From the first generation peptide fragment- based Protacs to the second generation of small molecule PROTAC designs that began in 2008, degraded target proteins range from the earliest methionyl aminopeptidase 2, androgen receptor, cellular retinoic acid binding protein, etc., to the most recent estrogen receptor, Tau microtubule-related proteins, kinases, etc. They have been used to treat diseases including cancer, rheumatoid, and neurodegenerative diseases. After the upsurge of small-molecule Protacs in 2015, Dr. Deshaies made the point that Protacs had the potential to be a major new drug and could surpass protein kinase inhibitors and monoclonal antibodies, two of the hottest areas of drug development. So far, BRD4, RIPK2, ERRα, BRD9, TBK1, Sirt2, CDK9, p38α, Pirin, c-Met, EGFR, FAK, FLT3 and other proteins have been reported to be degraded using PROTAC technology.

Currently, PROTAC is mainly used to discover new anticancer agents because they have unique advantages over classic inhibitors. Arvinas planned to launch a clinical trial of the PROTAC strategy for prostate cancer in 2019, which would last approximately 9 months. Arvinas has released the latest data on its PROTAC therapy: in two phase 1 clinical trials, its leading therapies ARV-110 and ARV-471 have achieved well-tolerated results. ARV-110 is a bifunctional molecule, one end of which can bind to a target-androgen receptor (AR) for this treatment in progress. The other end can bind to E3 ubiquitin ligase. Ligase can "tag" the target with ubiquitin, allowing the target protein to be degraded by the proteasomes that are transported to the cell. ARV-471 can degrade estrogen receptors and treat breast cancer. Not only that, Arvinas has also claimed an in vivo evidence that PROTAC can reduce the tau protein in the mouse brain. Injecting its tau protein degradation agent directly into the mouse hippocampus reduced the tau level by 50%. From this perspective, the PROTAC strategy (protein degradation instead of inhibition) can be used as a general and powerful treatment method for Alzheimer's disease and cancer in the future.


  1. Yutian, Zou, Danhui, Ma, Yinyin, & Wang. (2019). The Protac technology in drug development. Cell biochemistry and function.
  2. Gadd, M. S. , Testa, A. , Lucas, X. , Chan, K. H. , Chen, W. , & Lamont, D. J. , et al. (2017). Structural basis of Protac cooperative recognition for selective protein degradation. Nature Chemical Biology, 13(5), 514-521.

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