2139287-33-3
2139287-33-3
Chemical Structure
THAL-SNS-032
- CAS No.: 2139287-33-3
- Formula:C40H52N8O10S2
- Molecular Weight:869.02
IUPAC Name: N-(5-(((5-(tert-butyl)oxazol-2-yl)methyl)thio)thiazol-2-yl)-1-(14-((2-(2,6-dioxopiperidin-3-yl)-1,3-dioxoisoindolin-4-yl)amino)-2-oxo-6,9,12-trioxa-3-azatetradecyl)piperidine-4-carboxamide
InChIKey: BXDZOYLPNAIDOC-UHFFFAOYSA-N
SMILES: O=C(NCCOCCOCCOCCNC1=CC=CC(C(N2C(CC3)C(NC3=O)=O)=O)=C1C2=O)CN4CCC(C(NC5=NC=C(SCC6=NC=C(C(C)(C)C)O6)S5)=O)CC4
Biological Activity: THAL-SNS-032 is a selective CDK9 PROTAC degrader. THAL-SNS-032 recruits CRBN to form a ternary complex with CDK9, thereby triggering ubiquitination and proteasomal degradation of CDK9. THAL-SNS-032 also induces the degradation of CDK1, CDK2 and CDK7. THAL-SNS-032 elevates pH2AX levels, reduces MCL1s expression, and activates caspase-3. THAL-SNS-032 induces cancer cell apoptosis, regulates transcription, and inhibits the replication of human cytomegalovirus (CMV) and SARS-CoV-2. THAL-SNS-032 can be used in research related to breast cancer, leukemia, cytomegalovirus infection and SARS-CoV-2 infection[1][2][3].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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THAL-SNS-032 | 97.06% | THAL-SNS-032 is a selective CDK9 PROTAC degrader. THAL-SNS-032 recruits CRBN to form a ternary complex with CDK9, thereby triggering ubiquitination and proteasomal degradation of CDK9. THAL-SNS-032 also induces the degradation of CDK1, CDK2 and CDK7. THAL-SNS-032 elevates pH2AX levels, reduces MCL1s expression, and activates caspase-3. THAL-SNS-032 induces cancer cell apoptosis, regulates transcription, and inhibits the replication of human cytomegalovirus (CMV) and SARS-CoV-2. THAL-SNS-032 can be used in research related to breast cancer, leukemia, cytomegalovirus infection and SARS-CoV-2 infection. | ||||||||||||||||||||
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iVeliparib-AP6 | 99.84% | iVeliparib-AP6 is a proteolysis-targeting chimera (PROTAC) molecule designed based on Veliparib (HY-10129), which targets PARP1/2. The DC50s of iVeliparib-AP6 for inducing the degradation of PARP1 and PARP2 are 36 nM and 63 nM, respectively, and its IC50s are 69 nM and 21 nM, respectively. iVeliparib-AP6 contains a Veliparib-based PARP inhibitor warhead linked to a CRBN E3 ligase binder; it uses Thalidomide (HY-14658) as a ligand to recruit CRBN E3 ubiquitin ligase and exerts the PARP2 degradation mechanism. | ||||||||||||||||||||
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QC-01–175 | 99.94% | QC-01-175 is a Tau PROTAC degrader, with Kd values of 1.2 μM, 1.7 μM and 2.5 μM for wild-type, A152T mutant and P301L mutant tau-441 proteins, respectively. QC-01-175 binds to both Tau and CRBN, triggering ubiquitination and proteasomal degradation of Tau. QC-01-175 preferentially targets disease-associated Tau proteins in frontotemporal dementia. QC-01-175 inhibits MAO activity, with an IC50 of 8.56 μM. QC-01-175 suppresses the elevation of ROS levels. QC-01-175 can be used in studies related to frontotemporal dementia and amyotrophic lateral sclerosis. | ||||||||||||||||||||
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PROTAC eDHFR Degrader-1 | 98.09% | PROTAC eDHFR Degrader-1 is a PROTAC eDHFR degrader. PROTAC eDHFR Degrader-1 binds eDHFR-tagged proteins and Cereblon, thereby driving ternary complex formation, ubiquitination and proteasomal degradation. PROTAC eDHFR Degrader-1 degrades eDHFR-tagged proteins in multiple cell types and rodent models, and enables multiplex orthogonal protein regulation. PROTAC eDHFR Degrader-1 can be used in research related to metastatic ovarian cancer. | ||||||||||||||||||||
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PROTAC α-synuclein degrader 5 | 99.80% | PROTAC α-synuclein degrader 5 is a selective PROTAC degrader targeting α‑synuclein aggregates, with a DC50 of 7.51 μM. PROTAC α-synuclein degrader 5 binds to αSyn aggregates, recruits the CRBN E3 ubiquitin ligase, and mediates the ubiquitination and subsequent degradation of α‑synuclein aggregates. PROTAC α-synuclein degrader 5 activates the autophagy-lysosome pathway. PROTAC α-synuclein degrader 5 reduces ROS levels in neuroblastoma cells, restores mitochondrial membrane potential, rescues cell viability, and decreases LDH release. PROTAC α-synuclein degrader 5 degrades αSyn aggregates in Caenorhabditis elegans and ameliorates oxidative stress. PROTAC α-synuclein degrader 5 is used for the research of synucleinopathies, such as Parkinson's disease. | ||||||||||||||||||||
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PROTAC DYRK2 degrader 1 | 90.63% | PROTAC DYRK2 degrader 1 is a DYRK2 PROTAC degrader with DC50 values of 1.607 μM (MDA-MB-231 cells) and 3.265 μM (HeLa cells), respectively. PROTAC DYRK2 degrader 1 induces DYRK2 degradation via the ubiquitin-proteasome system. It is applicable to the research of triple-negative breast cancer and cervical cancer. | ||||||||||||||||||||
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PROTAC KDM3 degrader-1 | 99.07% | PROTAC KDM3 degrader-1 is a KDM3A/KDM3B PROTAC degrader with DC50 values of 13.73 nM and 172.6 nM in SW480 cells, respectively. PROTAC KDM3 degrader-1 induces cereblon-dependent proteasomal degradation of KDM3A and KDM3B. PROTAC KDM3 degrader-1 inhibits the oncogenic Wnt/β-catenin signaling pathway. PROTAC KDM3 degrader-1 eliminates colorectal cancer stem cells, suppresses their self-renewal, and blocks colony formation of colorectal cancer cells. PROTAC KDM3 degrader-1 inhibits tumor growth in a colorectal cancer xenograft mouse model. PROTAC KDM3 degrader-1 can be used for the research of colorectal cancer. | ||||||||||||||||||||
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PROTAC PDIA1 degrader 1 | PROTAC PDIA1 degrader 1 is a PDIA1 PROTAC degrader with a DC50 of 29.71 μM. PROTAC PDIA1 degrader 1 induces proteasome-dependent PDIA1 degradation via recruiting E3 ligase, ubiquitination and proteasomal degradation processes. PROTAC PDIA1 degrader 1 exhibits anticancer activity against breast cancer and epidermoid carcinoma. PROTAC PDIA1 degrader 1 can be used for the research of breast cancer and epidermoid carcinoma. | |||||||||||||||||||||
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PROTAC DYRK2 degrader-2 | 98.29% | PROTAC DYRK2 degrader-2 is a PROTAC DYRK2 degrader based on curcumin analog A3. It recruits the CRBN E3 ligase to mediate DYRK2 ubiquitination and achieves degradation via the ubiquitin-proteasome system. PROTAC DYRK2 degrader-2 downregulates the expression level of DYRK2 protein in cancer cells. It is applicable to cancer-related research. | ||||||||||||||||||||
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Thalidomide-NH-PEG3-NH-Boc | 97.26% | Thalidomide-NH-PEG3-NH-Boc is an E3 Ligase Ligand-Linker Conjugate consisting of Thalidomide (HY-14658) and NH-PEG3-NH-Boc. Thalidomide-NH-PEG3-NH-Boc acts as a ligand for Cereblon to recruit CRBN protein. The Boc protecting group at the end of Thalidomide-NH-PEG3-NH-Boc can be removed under acidic conditions to participate in the synthesis of PROTAC molecules. Thalidomide-NH-PEG3-NH-Boc is a key intermediate in the synthesis of CRBN-based PROTAC molecules. | ||||||||||||||||||||
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PROTAC Aster-A degrader-1 | PROTAC Aster-A degrader-1 is a PROTAC degrader targeting the sterol transporter (Aster-A), with a DC50 of 4.8 μM. PROTAC Aster-A degrader-1 binds to the sterol-binding domain of Aster-A, with a FI-Kd value of 83 nM. PROTAC Aster-A degrader-1 induces CRL- and proteasome-dependent degradation of Aster-A and inhibits autophagy in cancer cells. PROTAC Aster-A degrader-1 serves as a fluorescent probe. PROTAC Aster-A degrader-1 is useful for research related to cervical cancer, breast cancer, and lung adenocarcinoma. | |||||||||||||||||||||
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References
- [1]. Noblejas-López MDM, et al. Antitumoral Activity of a CDK9 PROTAC Compound in HER2-Positive Breast Cancer. International journal of molecular sciences. 2022 May 13;23(10):5476. [Content Brief]
- [2]. Olson CM, et al. Pharmacological perturbation of CDK9 using selective CDK9 inhibition or degradation. Nature chemical biology. 2018 Feb;14(2):163-170. [Content Brief]
- [3]. Hahn F, et al. Development of a PROTAC-Based Targeting Strategy Provides a Mechanistically Unique Mode of Anti-Cytomegalovirus Activity. International journal of molecular sciences. 2021 Nov 27;22(23):12858. [Content Brief]
