2. PROTAC Apoptosis MAPK/ERK Pathway
  3. PROTACs ASK1 p38 MAPK
  4. dASK1-VHL

dASK1-VHL is an orally active PROTAC degrader targeting ASK1. dASK1-VHL can effectively bind VHL and promote the selective degradation of ASK1. dASK1-VHL effectively reduces ASK1 protein levels, inhibits the activation of p38 MAPK, and reduces liver lipid content. dASK1-VHL provides new ideas for the study of Metabolic dysfunction-associated steatohepatitis (MASH) (Pink: ASK1 ligand 1 (HY-174860); Blue: E3 ligand (S,R,S)-AHPC (HY-125845); Black: Linker, (S,R,S)-AHPC-CO-C2-PEG-NHCO-C2-COOH (HY-174861).

For research use only. We do not sell to patients.

dASK1-VHL Chemical Structure

dASK1-VHL Chemical Structure

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dASK1-VHL Related Antibodies

Top Publications Citing Use of Products

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von Hippel-Lindau (VHL) Cereblon MDM2 cIAP1

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p38 MAPK p38α p38β MAPK13 p38δ p38γ

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Description

dASK1-VHL is an orally active PROTAC degrader targeting ASK1. dASK1-VHL can effectively bind VHL and promote the selective degradation of ASK1. dASK1-VHL effectively reduces ASK1 protein levels, inhibits the activation of p38 MAPK, and reduces liver lipid content. dASK1-VHL provides new ideas for the study of Metabolic dysfunction-associated steatohepatitis (MASH) (Pink: ASK1 ligand 1 (HY-174860); Blue: E3 ligand (S,R,S)-AHPC (HY-125845); Black: Linker, (S,R,S)-AHPC-CO-C2-PEG-NHCO-C2-COOH (HY-174861)[1].

In Vitro

dASK1-VHL (Compound dASK1-VHL) (1-1000 nM, 8 h) mediates efficient and specific ASK1 degradation via VHL E3 ligase in HepG2 cells[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

dASK1-VHL Related Antibodies

Western Blot Analysis[1]

Cell Line: HepG2 cells
Concentration: 1 nM, 10 nM, 50 nM, 100 nM, 500 nM, 1000 nM
Incubation Time: 8 h
Result: Achieved a 60 % degradation rate of ASK1 protein (at a concentration of 50 nM).
Was specific for VHL-mediated degradation, and pretreatment with VHL ligand VH032 completely abolished ASK1 degradation.
In Vivo

dASK1-VHL (Compound dASK1-VHL) (2 mg/kg, i.p, once daily for 14 days) degrades ASK1 through the ubiquitin-proteasome pathway, significantly improving the pathological characteristics of MASH in C57/Bl6 mice[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Male C57/Bl6 nude mice fed the MCD diet (4-6 weeks)[1]
Dosage: 2 mg/kg
Administration: Intraperitoneal injection (i.p.), once daily for 14 days
Result: Significantly reduced liver ASK1 protein and decreased p-p38 levels.
Caused no change in ASK1 mRNA and reduced ASK1 ubiquitination levels.
Reduced liver lipid accumulation.
Molecular Weight

986.10

Formula

C48H57F2N11O8S
SMILES

O=C(NC1=NC(C2=NN=CN2C(C)C)=CC=C1)C3=CC(NC(CCC(NCCOCCC(N[C@H](C(N4[C@@H](C[C@H](C4)O)C(NCC5=CC=C(C=C5)C6=C(N=CS6)C)=O)=O)C(C)(C)C)=O)=O)=O)=C(F)C=C3F
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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dASK1-VHL Related Classifications

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The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass   Concentration   Volume   Molecular Weight *
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The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

dASK1-VHLPROTACsASK1p38 MAPKApoptosis signal-regulating kinase 1MAP3K5MAPKKK5Mitogen-activated protein kinase kinase kinase 5MEK kinase 5HepG2 cellsC57BL/6MASHInhibitorinhibitorinhibit

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