PROTAC CDK9 degrader-12
PROTAC CDK9 degrader-12 is a selective CDK9 PROTAC degrader with a DC50 of 23 nM. PROTAC CDK9 degrader-12 induces proteasome-dependent degradation of CDK9, blocks CDK9-mediated HIV-1 transcriptional elongation, and reduces HIV-1 RNA synthesis. PROTAC CDK9 degrader-12 is applicable to research related to HIV-1 infection.
(Pink: CDK9 ligand (HY-181275); Blue: VHL ligand (HY-120217); Black: linker).
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- CAS No.: 3052648-82-2
- Formule: C60H82N14O7S2
- Masse moléculaire:1175.51
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
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Activité biologique
Description
IC50 & Target
[1]|
CDK9 23 nM () |
VHL |
In Vitro
PROTAC CDK9 degrader-12 (1.0 μM, unspecified serial dilutions; variable times) potently inhibits HIV-1 replication in SupT1 cells (IC50 = 78.92 nM) with a high selectivity index (531), acting by blocking CDK9-mediated HIV-1 transcription elongation, and its anti-HIV-1 activity is dependent on wild-type CDK9 degradation[1].
PROTAC CDK9 degrader-12 (10 μM; 24 h) exhibits no obvious cytotoxicity in HepG2 cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 3052648-82-2
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Masse moléculaire 1175.51
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Formule C60H82N14O7S2
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SMILES
CC1=C(C2=CC=C(CNC([C@@H]3C[C@@H](O)CN3C([C@@H](NC(CCCCCCCCCCN4N=NC(CN5CCN(S(=O)(C6=CC=C(NC7=NC8=C(C=N7)C=C(C(N(C)C)=O)N8C9CCCC9)C=C6)=O)CC5)=C4)=O)C(C)(C)C)=O)=O)C=C2)SC=N1
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
PROTAC CDK9 degrader-12 Related Classifications
HY-181231 Related Classifications
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