- Signaling Pathways
- PROTAC
- PROTACs
PROTACs
PROTAC (PROteolysis-TArgeting Chimera) is a heterobifunctional nanomolecule containing two different ligands, ligand for ubiquitin E3 and ligand for target protein. The two parts are connected by linker to form a "three-unit" polymer, target protein ligand-linker-E3 ligase ligand. Building blocks of PROTAC molecules include PROTAC Linker, Ligand for Target Protein for PROTAC, Ligand for E3 Ligase, E3 Ligase Ligand-Linker Conjugate, Target Protein Ligand-Linker Conjugate, etc.
PROTACs Isoform Specific Products
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PROTACs Related Products (1321)
Related Products (1321)
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Antibodies (1)
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PROTACs Isoform Comparison
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BTX-6654 formate
0 ImagesCat. No.: HY-161233APurity: 98.85% -
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L18I
0 ImagesL18I is a Bruton's tyrosine kinase (BTK) PROTAC degrader that targets wild-type and BTKC481, and recruits the cereblon E3 ligase to mediate proteasomal degradation. L18I regulates the BCR, TLR, FcγR and NLRP3 inflammasome signaling pathways, inhibits the phosphorylation of PLCγ-2, ERK1/2 and p38, and reduces the levels of B cell activation markers CD25, CD69 and CD86. L18I downregulates the NF-κB, TNF and TLR signaling pathways, reduces the production of pro-inflammatory cytokines, and decreases immune cell infiltration and immune complex deposition. L18I inhibits the proliferation of BTK-expressing lymphoma cells, induces tumor regression in xenograft models, and exhibits synergistic activity when combined with inhibitors of SYK, PI3K or Lyn. L18I can be used in research related to lupus, diffuse alveolar hemorrhage and B-cell lymphoma. -
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PROTAC USP39 Degrader-1
0 ImagesCat. No.: HY-180907Purity: 98.61%PROTAC USP39 Degrader-1 (compound USP39_PROTAC_V1) is a potent and selective PROTAC USP39 degrader. PROTAC USP39 Degrader-1 induces degradation of USP39 by recruiting the VHL E3 ligase via a hydroxyl-proline-containing ligand, forming a ternary complex with a Kd of 232 nM. PROTAC USP39 Degrader-1 degrades USP39 in a VHL-, proteasome-, and the neddylation pathway-dependent manner. -
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MS181
0 ImagesMS181 is a BMI1 and RING1B degrader with antiproliferative activity. MS181 induces degradation via an EED-, CRBN-, and ubiquitin-proteosome system-dependent pathway, with preferential targeting over PRC2 components. MS181 acts in VHL-defective cancer cells. MS181 serves as a chemical biology tool to study PRC1 roles in cancer. MS181 can be used for the research of myelogenous leukemia, renal cell carcinoma, metastatic prostate cancer, triple negative breast cancer. -
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- SR-1114
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- PROTAC ERα Degrader-2
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- PROTAC MDM2 Degrader-3
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TL13-12
0 ImagesTL13-12 is a potent and selective ALK-PROTAC degrader and inhibits ALK activity with an IC50 value of 0.69 nM. TL13-12 also prompts the degradation of additional kinases including Aurora A, FER, PTK2, and RPS6KA1 with IC50 values of 13.5 nM, 5.74 nM, 18.4 nM, and 65 nM, respectively. TL13-12 is comprised of the conjugation of TAE684 (HY-10192) and the Cereblon ligand of Pomalidomide (HY-10984). -
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- PROTAC Bcl-xL degrader-2
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- SZUH280
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- PROTAC BRD9 Degrader-1
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- PROTAC FKBP Degrader-3
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PROTAC PARP1 degrader
0 ImagesPROTAC PARP1 degrader is a PROTAC PARP1 degrader. PROTAC PARP1 degrader mediates the interaction between PARP1 and MDM2 E3 ubiquitin ligase, thereby inducing ubiquitination of PARP1 and subsequent proteasome-mediated degradation. PROTAC PARP1 degrader selectively inhibits the growth of breast cancer cells. PROTAC PARP1 degrader induces cell apoptosis by activating caspase-3 and phosphatidylserine externalization. PROTAC PARP1 degrader can be used in the research of triple-negative breast cancer. -
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INY-03-041 trihydrochloride
0 ImagesCat. No.: HY-133120AINY-03-041 trihydrochloride is a potent, highly selective and PROTAC-based pan-AKT degrader consisting of the ATP-competitive AKT inhibitor Ipatasertib (HY-15186) conjugated to Lenalidomide (HY-A0003). INY-03-041 trihydrochloride inhibits AKT1, AKT2 and AKT3 with IC50s of 2.0, 6.8 and 3.5 nM, respectively. -
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- AT6
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CCT367766 formic
0 ImagesCat. No.: HY-122653APurity: 98.10%CCT367766 formic is a potent and the third generation heterobifunctional and Cereblon-based pirin targeting protein degradation probe (PDP, or PROTAC), depletes pirin protein expression at low concentration. CCT367766 formic exhibits a moderate affinity for the CRBN-DDB1 complex with an IC50 value of 490 nM. CCT367766 formic reveals a good affinity for the recombinant pirin and CRBN with Kd values of 55 nM and 120 nM, respectively. CCT367766 formic provides a potential chemical tool to study a largely unexplored protein. -
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DD-03-171
0 ImagesDD-03-171 is a PROTAC BTK degrader. DD-03-171 inhibits mantle cell lymphoma (MCL) cell proliferation (IC50 = 5.1 nM) and prolongs the survival of mice bearing a lymphoma PDX model by degrading BTK, IKFZ1, and IKFZ3. DD-03-171 also inhibits platelet function and thrombosis. (Pink: BTK ligand 9 (HY-168292); Black: linker (HY-28875); Blue: Thalidomide-NH-CH2-COOH (HY-131717)). -
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RJS308 TFA
0 ImagesCat. No.: HY-173011APurity: 98.36%RJS308 TFA is a selective Cyclophilin A (CypA) PROTAC degrader. RJS308 TFA induces ubiquitin-dependent CypA degradation by recruiting the VHL E3 ligase complex, and forms a ternary complex with CypA and VHL/elongin C/elongin B. RJS308 TFA exhibits anti-HIV-1 and anti-HCV activities. RJS308 TFA can be used in studies related to viral infections. -
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22-SLF
0 ImagesCat. No.: HY-163807CAS No.: 3079209-82-522-SLF is a PROTAC degrader, that degrades FK506-binding protein 12 (FKBP12) with a DC50 of 0.5 µM. 22-SLF interacts with C227 and C228 in FBXO22 to induce a ternary complex between FKBP12 and FBXO22, and degrades FKBP12 in a FBXO22-dependent manner. 22-SLF can be used for fundamental cancer research as a probe to study the FBXO22 degradation pathway. -
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ARD-2051
0 ImagesARD-2051 is a selective and orally active androgen receptor (AR) PROTAC degrader. ARD-2051 achieves DC50 values of 0.6 nM for AR protein degradation in both the LNCaP and VCaP prostate cancer cell lines. ARD-2051 exhibits effective anti-tumor activity in VCaP xenograft mice model. ARD-2051 can be used for the research of prostate cancer. -
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