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PROTAC degraders recruit an E3 ubiquitin ligase to a target protein so that the proteasome degrades it. Each proteolysis-targeting chimera (PROTAC) links a target-binding ligand to an E3 ligase ligand through a chemical linker. The approach was first described in 2001, and later work showed that small-molecule PROTACs can act catalytically, removing several target copies per molecule. Examples include the bromodomain and extra-terminal (BET) degraders dBET1, MZ1 and ARV-771, and the estrogen receptor degrader ERD-308. Degraders of anti-apoptotic proteins, such as PROTAC Mcl1 degrader-1, are also listed.
xStAx-VHLL is a PROTAC degrader targeting β-catenin, promoting its ubiquitination and proteasomal degradation. It effectively inhibits the Wnt/β-catenin signaling pathway and suppresses proliferation of colon cancer cells, demonstrating anti-tumor activity.
DAS-5-oCRBN is a selective and potent PROTAC degrader of c-Src kinase, acting through CRBN-mediated ubiquitination. It effectively reduces c-Src levels and inhibits proliferation in c-Src-dependent cancer cell lines, making it a useful tool for targeted protein degradation research.
MS9427 TFA is a potent PROTAC degrader targeting EGFR, with binding affinities (K_d) of 7.1 nM for wild-type EGFR and 4.3 nM for the EGFR L858R mutant. It selectively degrades the mutant EGFR via both the ubiquitin–proteasome system (UPS) and autophagy–lysosome pathways. MS9427 TFA effectively inhibits the proliferation of non-small cell lung cancer (NSCLC) cells and is a valuable tool for anticancer research focused on EGFR-driven malignancies.
SMD-3040 formate is a potent and selective PROTAC degrader targeting SMARCA2, a core ATPase subunit of the SWI/SNF chromatin remodeling complex. It exhibits strong in vivo antitumor activity, making it a promising candidate for cancer research involving epigenetic regulation and synthetic lethality strategies.
LL-K8-22 is a potent, selective, and durable PROTAC degrader targeting the CDK8–cyclin C complex, with DC₅₀ values of 2.52 μM and 2.64 μM, respectively. It suppresses STAT1 Ser727 phosphorylation and inhibits E2F- and MYC-driven oncogenic transcriptional programs. LL-K8-22 shows potential for use in triple-negative breast cancer (TNBC) research and related therapeutic studies.
MS15 TFA is a potent and selective PROTAC degrader targeting AKT isoforms. It inhibits the activity of AKT1, AKT2, and AKT3 with IC₅₀ values of 798 nM, 90 nM, and 544 nM, respectively. MS15 TFA serves as a valuable tool for studying AKT signaling and its role in cancer and metabolic diseases.
PROTAC NCOA4 Degrader-1 (Compound V3) is a highly potent PROTAC targeting NCOA4, with a DC₅₀ of 3 nM in HeLa cells. It functions as a ferroptosis inhibitor by reducing NCOA4 levels and lowering intracellular ferrous iron (Fe²⁺) concentrations. PROTAC NCOA4 Degrader-1 has demonstrated protective effects in a CCl₄-induced acute liver injury model, making it a valuable tool for studying ferroptosis and liver disease therapeutics.
SS47 TFA is a PROTAC-based degrader targeting hematopoietic progenitor kinase 1 (HPK1), an immunosuppressive regulatory kinase. It induces proteasome-mediated degradation of HPK1 and significantly enhances the antitumor efficacy of BCMA CAR-T cell therapy in vivo. In addition to its biological function, SS47 TFA is also a click chemistry reagent containing an alkyne group, allowing it to participate in copper-catalyzed azide–alkyne cycloaddition (CuAAC) with azide-functionalized molecules. This dual functionality makes SS47 TFA a valuable tool in both cancer immunotherapy research and chemical biology applications.
SJ1008030 (Compound 8) formic is a selective PROTAC degrader of JAK2, designed to target and eliminate JAK2 protein via the ubiquitin–proteasome pathway. It effectively inhibits the growth of MHH–CALL-4 leukemia cells with an IC₅₀ of 5.4 nM. SJ1008030 formic is a valuable tool for leukemia research and the study of JAK2-driven signaling pathways.
dAURK-4 hydrochloride is a potent and selective PROTAC degrader targeting Aurora A kinase (AURKA), derived from the AURKA inhibitor Alisertib. It effectively induces AURKA degradation and exhibits notable anticancer activity, making it a valuable agent for studying AURKA-driven oncogenic pathways and therapeutic development.
SIAIS164018 hydrochloride is a PROTAC-based dual degrader targeting ALK and EGFR, with IC₅₀ values of 2.5 nM for ALK and 6.6 nM for the ALK G1202R mutant. It effectively suppresses cancer cell migration and invasion, induces G1 phase cell cycle arrest, and promotes apoptosis, making it a promising candidate for targeted cancer therapy research.
PROTAC EZH2 Degrader-2 (Compound E-3P-MDM2) is a PROTAC molecule designed by linking the EZH2 inhibitor Tazemetostat (EPZ6438) to an E3 ligase ligand. It induces dose-dependent degradation of EZH2 in SU-DHL-6 cells, suppresses H3K27me3 expression, and concurrently degrades PRC2 components EED and SUZ12 without altering their mRNA levels. PROTAC EZH2 Degrader-2 exhibits strong anti-cancer and anti-proliferative activity, making it a valuable tool for epigenetic and oncology research.
CCT367766 formic is a third-generation, cereblon-based heterobifunctional PROTAC and pirin-targeting protein degradation probe (PDP). It effectively depletes pirin protein expression at low concentrations. CCT367766 formic demonstrates moderate affinity for the CRBN–DDB1 complex (IC₅₀ = 490 nM) and strong binding affinity for recombinant pirin and CRBN, with K_d values of 55 nM and 120 nM, respectively. This compound serves as a valuable chemical tool for exploring the biological roles of the largely understudied protein pirin.
PROTAC CDK12/13 Degrader-1 (7f) is a highly selective dual degrader targeting CDK12 and CDK13, with DC₅₀ values of 2.2 nM and 2.1 nM, respectively. It exhibits potent anti-proliferative activity and serves as a valuable tool for investigating transcriptional regulation and therapeutic strategies in breast cancer research.
MS9715 is a potent and selective PROTAC degrader targeting NSD3, designed by conjugating the NSD3 PWWP1 domain binder BI-9321 to a von Hippel-Lindau (VHL) E3 ligase ligand. It effectively induces degradation of NSD3 and holds significant potential for research in NSD3-dependent cancers, offering a novel approach to target epigenetic drivers in oncology.
MS181 (Compound 1) is a potent PROTAC degrader that targets components of the polycomb repressive complex 1 (PRC1) by recruiting cereblon (CRBN) and binding EED. It effectively reduces the expression of key PRC1 and PRC2 components, including EED, EZH2, SUZ12, BMI1, and RING1B. MS181 exhibits significant antiproliferative activity, making it a valuable tool for studying epigenetic regulation and potential cancer therapeutics.
PROTAC SOS1 Degrader-1 (TFA) is a potent PROTAC molecule targeting SOS1, with a DC₅₀ of 98.4 nM. It exhibits antiproliferative activity in cancer cells harboring various KRAS mutations and demonstrates antitumor efficacy with low toxicity, making it a promising candidate for targeted cancer therapy research.
MDEG-541 is a potent PROTAC degrader targeting the MYC-MAX complex, derived from the MYC-MAX dimerization inhibitor 10058-F4 (28RH) and thalidomide as the cereblon-recruiting ligand. It exhibits strong antiproliferative activity and reduces the expression of key oncogenic and regulatory proteins, including GSPT1, MYC, GSPT2, and PLK1. MDEG-541 is a valuable tool for studying MYC-driven cancers and targeted protein degradation strategies.
ARM165 is a heterobifunctional PROTAC molecule that targets and degrades PIK3CG (PI3Kγ), effectively inhibiting the PI3Kγ-Akt signaling pathway. It exhibits potent antileukemic activity, suppressing the proliferation of acute myeloid leukemia (AML) cells with an IC₅₀ of less than 1 μM. ARM165 is a promising tool for investigating PI3Kγ-driven signaling and developing targeted therapies for leukemia.
MS8709 (compound 10) is a first-in-class PROTAC degrader targeting the histone methyltransferases G9a and GLP, with potential anticancer activity. Engineered from the G9a/GLP inhibitor UNC0642, MS8709 recruits the von Hippel–Lindau (VHL) E3 ubiquitin ligase to promote the selective ubiquitination and proteasomal degradation of G9a/GLP proteins. This targeted degradation approach offers a novel therapeutic strategy for disrupting epigenetic dysregulation in cancer.
SJ995973 is a highly potent PROTAC (proteolysis-targeting chimera) designed to selectively degrade bromodomain and extra-terminal domain (BET) family proteins, including BRD2, BRD3, and BRD4. By inducing targeted proteasomal degradation, SJ995973 enables efficient disruption of BET protein function, offering a powerful approach for investigating BET-related transcriptional regulation and for the development of novel anticancer therapies.
SJF-1521 is a selective PROTAC degrader targeting the epidermal growth factor receptor (EGFR). It incorporates lapatinib, a known EGFR inhibitor, as the targeting ligand and promotes proteasomal degradation of EGFR. SJF-1521 effectively induces EGFR degradation in OVCAR8 ovarian cancer cells, offering a promising strategy for disrupting EGFR signaling in EGFR-driven malignancies.
ARD-61 is a highly potent and selective PROTAC degrader of the androgen receptor (AR), also capable of degrading progesterone receptors (PR) in AR-positive cancer cell lines. It induces apoptosis and demonstrates significant antitumor efficacy in vivo, effectively inhibiting tumor growth in the MDA-MB-453 xenograft mouse model. Additionally, ARD-61 is equipped with an alkyne functional group, enabling its use as a click chemistry reagent through copper-catalyzed azide-alkyne cycloaddition (CuAAC) with azide-containing molecules, facilitating conjugation and functionalization for chemical biology applications.
dBET23 is a highly potent and selective PROTAC degrader targeting the bromodomain-containing protein BRD4. It exhibits a DC₅₀ of approximately 50 nM at 5 hours for the BRD4 bromodomain 1 (BRD4^BD1) protein, effectively promoting its ubiquitination and proteasomal degradation. dBET23 serves as a valuable chemical tool for studying BRD4-dependent transcriptional regulation and holds potential for therapeutic applications in BRD4-driven cancers.
PP-C8 is a potent and selective PROTAC degrader targeting the CDK12–Cyclin K complex. It induces efficient degradation of CDK12 and Cyclin K with DC₅₀ values of 416 nM and 412 nM, respectively. In preclinical models, PP-C8 exhibits strong synergistic antiproliferative effects when combined with PARP inhibitors, particularly in triple-negative breast cancer (TNBC), highlighting its potential as a therapeutic strategy for enhancing DNA damage response–targeted treatments.
