rG4 WT_AHPC_PEG2
rG4 WT_AHPC_PEG2 is a selective RNA G-quadruplex-based DHX36 PROTAC degrader with a Kd value of 79.7 nM. rG4 WT_AHPC_PEG2 degrades DHX36 via a proteasome-dependent mechanism, without significantly degrading other G4-binding proteins including NCL, DHX9, hnRNP, SRSF and FMR1.
(Pink: Target protein ligand; Blue: VHL ligand (HY-125845); Black: linker).
For research use only. We do not sell to patients.
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Storage:
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
All PROTACs Isoforms
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Biological Activity
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VHL |
rG4 WT_AHPC_PEG2 (30 nM; 30 min) binds to the RHAU53 peptide with a Kd of 67.5 nM, demonstrating strong molecular recognition of the DHX36 fragment[1].
rG4 WT_AHPC_PEG2 (40 nM; 30 min) binds to full-length DHX36 protein with a Kd of 79.7 nM, verifying robust target recognition[1].
rG4 WT_AHPC_PEG2 (3.75-500 nM; 24 h) induces proteasome-dependent degradation of DHX36 in HeLa cells, achieving over 90% degradation at 62.5 nM after 24 h and >50% degradation within 6 h at 50 nM[1].
rG4 WT_AHPC_PEG2 (15.6-500 nM; 24 h) reduces endogenous APP protein levels in HeLa cells in a concentration-dependent manner, correlating with DHX36 degradation[1].
rG4 WT_AHPC_PEG2 (50-200 nM; 24 h) induces proteasome-dependent degradation of DHX36 and concentration-dependent reduction of Gnai2 protein in mouse C2C12 myoblast cells[1].
rG4 WT_AHPC_PEG2 (200 nM; 24 h) impairs the proliferative capacity of mouse C2C12 myoblast cells and skeletal muscle stem cells by reducing EdU incorporation[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HeLa cells
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Concentration:3.75-500 nM (dose-dependent assay); 50 nM (time-dependent assay); 50 nM + 1 μM MG132 (proteasome inhibition assay)
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Incubation Time:24 h (dose-dependent assay); 0-48 h (time-dependent assay); 24 h (proteasome inhibition assay)
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Result:Induced dose-dependent degradation of DHX36, with over 90% degradation observed at 62.5 nM after 24 h, followed by a hook effect at higher concentrations.
Reduced DHX36 by >50% within 6 h of 50 nM treatment, with maximal degradation (~95%) at 48 h.
Blocked DHX36 degradation was observed with co-treatment with MG132, confirming proteasome-dependent activity.
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Cell Line:HeLa cells
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Concentration:15.6-500 nM
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Incubation Time:24 h
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Result:Induced concentration-dependent reduction of endogenous APP protein, which correlated with DHX36 degradation (maximal DHX36 and APP reduction at 62.5 nM).
Caused a slight increase in APP levels at higher concentrations, consistent with the hook effect.
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Cell Line:mouse C2C12 myoblast cells
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Concentration:50-200 nM (dose-dependent assay); 200 nM + 1 μM MG132 (proteasome inhibition assay)
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Incubation Time:24 h
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Result:Induced dose-dependent degradation of DHX36, with significant reduction observed at 100 nM, 150 nM, and 200 nM.
Reduced Gnai2 protein levels in parallel with DHX36 degradation, with significant reduction at 100 nM and 200 nM.
Blocked DHX36 degradation and preserved Gnai2 levels were observed with co-treatment with MG132.
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Cell Line:mouse C2C12 myoblast cells, skeletal muscle stem cells (SCs)
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Concentration:200 nM
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Incubation Time:24 h; 3 h (EdU treatment)
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Result:Reduced the percentage of EdU-positive C2C12 cells from 55.06% to 44.33%.
Reduced the percentage of EdU-positive SCs from 3.70% to 2.47%.
Chemical Information
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Appearance Solid
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SMILES
[rG4 WT_AHPC_PEG2]
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)