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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.
MTX-23 is an androgen receptor (AR)-targeting PROTAC that degrades both AR-FL and the splice variant AR-V7. It effectively inhibits prostate cancer cell proliferation and induces apoptosis, making it a promising tool for studying AR signaling and therapeutic resistance in prostate cancer.
LC-2 is a first-in-class, VHL-based PROTAC designed to degrade endogenous KRAS G12C. Incorporating a MRTX849-derived covalent warhead, LC-2 binds KRAS G12C and recruits the VHL E3 ligase, inducing rapid and sustained degradation with DC₅₀ values between 0.25 and 0.76 μM. It effectively suppresses MAPK signaling in both homozygous and heterozygous KRAS G12C mutant cell lines, making it a valuable tool for targeted cancer research.
INY-03-041 is a potent and highly selective PROTAC-based pan-AKT degrader that targets AKT1, AKT2, and AKT3 with IC₅₀ values of 2.0 nM, 6.8 nM, and 3.5 nM, respectively. It is composed of the ATP-competitive AKT inhibitor GDC-0068 linked to the cereblon ligand lenalidomide, making it a valuable tool for studying AKT signaling and targeted cancer therapy.
C-02 is a PROTAC molecule composed of the hexokinase inhibitor lonidamine linked to the cereblon ligand thalidomide. It selectively degrades hexokinase 2 in 786-O and PANC-1 cells at 20 µM. C-02 exhibits cytotoxicity across multiple cancer cell lines, with IC₅₀ values of 34.07 µM (786-O), 5.08 µM (4T1), 31.53 µM (PANC-1), 6.11 µM (HGC-27), and 21.65 µM (MCF-7), supporting its use in cancer metabolism research.
XL01126 is a potent PROTAC degrader of LRRK2, with DC₅₀ values of 14 nM for the G2019S mutant and 32 nM for wild-type LRRK2. It is blood-brain barrier permeable, making it a valuable tool for Parkinson’s disease research. XL01126 enables investigation of both catalytic and non-catalytic functions of LRRK2.
BSJ-4-116 is a PROTAC molecule derived from a modified form of the multi-kinase degrader TL12-186, linked to a cereblon ligand and E3 ligase ligand intermediate. It induces time- and concentration-dependent degradation of CDK12 in Jurkat T cells and downregulates genes involved in DNA double-strand break repair at 50 nM. BSJ-4-116 also inhibits MOLT-4 leukemia cell growth in a cereblon-dependent manner, supporting its application in cancer and DNA repair research.
SK-575 is a highly potent and selective PROTAC degrader of PARP1, with an IC₅₀ of 2.30 nM. It effectively inhibits the proliferation of cancer cells harboring BRCA1/2 mutations, making it a valuable agent for targeted cancer research.
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dTAGV-1 TFA is a potent and selective degrader of FKBP12^F36V-tagged fusion proteins. It enables efficient in vivo degradation of FKBP12^F36V-Nluc, making it a valuable tool for conditional protein degradation studies in live models.
PROTAC EZH2 Degrader-1 (Compound 150d) is a potent PROTAC molecule targeting EZH2, with an IC₅₀ of 2.7 nM for inhibition of its methyltransferase activity. By degrading EZH2, it provides a valuable tool for studying its role in tumorigenesis and cancer progression.
Synonyms: BTK-IN-24
NX-5948 (BTK-IN-24) is an orally bioavailable, blood-brain barrier-penetrant PROTAC degrader targeting Bruton's tyrosine kinase (BTK). It induces BTK degradation via the cereblon E3 ligase pathway, effectively inhibiting B cell activation. NX-5948 exhibits both anti-inflammatory and antitumor activities, supporting its use in cancer and immune-related research.
MS432 is a first-in-class, highly selective PROTAC degrader targeting MEK1 and MEK2, based on PD0325901 and a von Hippel-Lindau (VHL) E3 ligase ligand. It demonstrates favorable plasma exposure in mice and induces MEK1 and MEK2 degradation in HT29 cells with DC₅₀ values of 31 nM and 17 nM, respectively.
FHD-609 is a PROTAC degrader and inhibitor of BRD9, a key component of the non-canonical BAF (ncBAF) chromatin remodeling complex. It is designed for studying cancers harboring mutations in BAF complex subunits. FHD-609 shows potential in adrenocortical carcinoma (ACC) treatment, particularly in combination with Telomelysin or INO5401.
UNC6852 is a selective PROTAC degrader of the polycomb repressive complex 2 (PRC2), incorporating ligands for EED (embryonic ectoderm development) and von Hippel-Lindau (VHL). It targets EED with an IC₅₀ of 247 nM, enabling PRC2 degradation and serving as a valuable tool for epigenetic and cancer research.
JET-209 is a potent PROTAC degrader targeting CBP and p300, with DC₅₀ values of 0.05 nM and 0.2 nM, respectively. It is composed of lenalidomide, a linker, and the bromodomain inhibitor GNE-207. JET-209 is a valuable tool for cancer research involving epigenetic regulation.
PIK5-12d is a potent PROTAC degrader targeting PIKfyve, with a DC₅₀ of 1.48 nM. It induces extensive cytoplasmic vacuolization, disrupts autophagic flux, and inhibits proliferation in multiple prostate cancer cell lines. PIK5-12d exhibits notable anti-tumor activity, supporting its use in cancer research.
PROTAC CDK12/13 Degrader-1 (7f) TFA is a highly selective dual degrader of CDK12 and CDK13, with DC₅₀ values of 2.2 nM and 2.1 nM, respectively. It exhibits strong antiproliferative activity and is a valuable tool for investigating cell cycle regulation and therapeutic strategies in breast cancer research.
MYC-RIBOTAC is a ribonuclease-targeting chimera (RIBOTAC) designed to degrade MYC mRNA by targeting its internal ribosome entry site (IRES). It combines a MYC mRNA-binding moiety with a small molecule that recruits and activates RNase L1. MYC-RIBOTAC reduces MYC mRNA and protein levels, induces apoptosis, and holds promise for antitumor research.
FOSL1 Degrader 1 (4) is a potent T-5224-based PROTAC that selectively degrades FOSL1 (AP-1), suppressing cancer stemness gene expression in head and neck squamous cell carcinoma (HNSCC). It effectively inhibits tumor growth and eliminates cancer stem cells, showing 30–100 times greater efficacy than T-5224.
SIAIS100 TFA is a potent PROTAC degrader targeting BCR-ABL, with a DC₅₀ of 2.7 nM. It is a valuable tool for studying BCR-ABL signaling and therapeutic strategies in chronic myeloid leukemia (CML).
JPS016 is a benzamide-based PROTAC that recruits the Von Hippel-Lindau (VHL) E3 ligase to selectively degrade class I histone deacetylases (HDACs). It is a potent degrader of HDAC1/2, leading to broad transcriptional changes and enhanced apoptosis in HCT116 cells, supporting its application in epigenetic and cancer research.
BSJ-03-204 triTFA is a potent and selective PROTAC degrader targeting CDK4/6, constructed using ligands for cereblon and CDK. Based on Palbociclib, it exhibits IC₅₀ values of 26.9 nM for CDK4/D1 and 10.4 nM for CDK6/D1. BSJ-03-204 triTFA does not induce IKZF1/3 degradation and shows anti-cancer activity, making it a valuable tool for cell cycle and oncology research.
U7D-1 is a first-in-class, potent, and selective PROTAC degrader of USP7 (ubiquitin-specific protease 7), with a DC₅₀ of 33 nM in RS4;11 cells. It exhibits anticancer activity and induces apoptosis in Jeko-1 cells, supporting its utility in cancer research targeting deubiquitinating enzymes.
PROTAC IRAK3 Degrader-1 (Compound 23) is a potent and selective PROTAC molecule targeting IRAK3, with an IC₅₀ of 5 nM. It enables efficient degradation of IRAK3, providing a valuable tool for studying innate immune signaling and inflammatory pathways.
dFKBP-1 is a potent PROTAC-based degrader targeting FKBP12. It is composed of the FKBP12-binding ligand SLF, a thalidomide-derived cereblon ligand, and a linker. dFKBP-1 enables selective degradation of FKBP12 via the CRBN-mediated ubiquitin-proteasome pathway.
PROTAC RIPK Degrader-2 is a non-peptidic, VHL-based PROTAC that selectively targets the serine/threonine kinase RIPK2 for degradation. It promotes cancer cell death and ion channel activation, while also inhibiting key protein interactions involved in disease pathways, including those related to cancer and diabetes.
