PROTAC AR Degrader-13
PROTAC AR Degrader-13 is a proteolysis-targeting chimera (PROTACs) that targets the androgen receptor (AR). PROTAC AR Degrader-13 has a DC50 of 0.90 nM in LNCaP cells and a DC50 of 0.23 nM in hDPC cells. PROTAC AR Degrader-13 induces AR degradation, downregulates TGF-β1 expression, upregulates β-catenin levels, and restores the Wnt/β-catenin pro-proliferation signaling in hair follicles. In a testosterone-induced androgenetic alopecia mouse model, PROTAC AR Degrader-13 accelerates hair regeneration rate, increases hair density and hair diameter. PROTAC AR Degrader-13 can be used for the research of androgenetic alopecia.
For research use only. We do not sell to patients.
- Formula: C39H44ClF3N10O6
- Molecular Weight:841.28
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
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Biological Activity
Description
IC50 & Target
[1]|
Cereblon |
In Vitro
PROTAC AR Degrader-13 (dAR-6-1) potently degrades androgen receptor in LNCaP cells with a DC50 of 0.90 nM and a Dmax of 91%[1].
PROTAC AR Degrader-13 (0.1-1000 nM; 0.5-36 h) potently degrades androgen receptor in hDPC cells with a DC50 of 0.23 nM and a Dmax of 90% via a CRBN-, ubiquitin-proteasome system-, and ternary complex-dependent mechanism[1].
PROTAC AR Degrader-13 (0.1-500 μM; 72 h) does not significantly inhibit hDPC cell viability, with an IC50 > 500 μM after 72 h of treatment[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:human dermal papilla (hDPC) cells
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Concentration:0.1, 0.3, 1, 3, 10, 30, 100, 300, 1000 nM (6 h incubation)
10 nM (time-course incubations)
1, 10, 100 nM (4 h incubation with siRNA pretreatment)
1, 10, 100 nM (4 h incubation with inhibitor/ligand pretreatment) -
Incubation Time:6 h (0.1-1000 nM)
0.5, 1, 2, 3, 4, 6, 9, 12, 24, 36 h (10 nM)
4 h -
Result:Induced rapid, sustained AR degradation, detectable within 2 h and maintained for over 36 h at 10 nM.
Exhibited dose-dependent degradation across 0.1-1000 nM without a hook effect, with a DC50 of 0.23 nM and a Dmax of 90%.
Abrogated degradation occurred with CRBN knockdown, while pretreatment with MG-132 (HY-13259), Pevonedistat (HY-70062), lenalidomide (HY-A0003), or enzalutamide (HY-70002) blocked degradation.
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Cell Line:hDPC cells
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Concentration:0.01, 0.1, 1, 10, 100, 1000 μM
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Incubation Time:72 h
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Result:Did not induce significant growth inhibition, with cell viability remaining above ~90% at concentrations up to 100 μM, ~80% at 100−500 μM, and an IC50 > 500 μM.
Parmacokinetics
| Species | Dose | Route | CL | T1/2 | Tmax | Cmax | C0 | AUClast | AUC0-∞ | MRTINF_obs | Vz |
|---|---|---|---|---|---|---|---|---|---|---|---|
| Mice[1] | 2 mg/kg | i.v. | 10.1 mL/min/kg | 1.79 h | 0.083 h | 1019 ng/mL | 1208 ng/mL | 3465 ng·h/mL | 3487 ng·h/mL | 3.96 h | 1.39 L/kg |
In Vivo
PROTAC AR Degrader-13 (1-100 mg/mL; topical) in C57BL/6 mice results in concentration-dependent skin retention[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (male, 6 weeks old, depilated on dorsal skin, treated daily with 0.5% testosterone solution to induce follicular miniaturization)[1]
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Dosage:100 mg/mL
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Administration:topical; once daily or once every 3 days; 28 days
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Result:Triggered prominent hair coverage on day 10-11, showing superior hair coverage versus minoxidil at day 12, 14 and 16.
Achieved hair density equivalent to minoxidil, with both groups exhibiting higher hair density and distinctly enlarged hair diameter compared to the AGA model after daily topical use for 28 days.
Delivered hair regrowth potency comparable to minoxidil, with notably raised hair density and thickened hair diameter against the AGA model under triweekly administration.
Evoked no observable cutaneous irritation or histopathological lesions.
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Animal Model:C57BL/6 (male, 6 weeks old)[1]
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Dosage:1 mg/mL; 10 mg/mL; 100 mg/mL
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Administration:topical
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Result:Exhibited concentration-dependent skin retention, with 1 mg/mL formulation showing minimal retention, 10 mg/mL formulation presenting moderate retention, and 100 mg/mL formulation reaching the peak retention of 2900 ng/cm2.
Chemical Information
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Molecular Weight 841.28
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Formula C39H44ClF3N10O6
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SMILES
ClC1=CC(O[C@H]2CC[C@@H](CC2)NC(C3=CC=C(N=N3)N4CCC(CC4)C[NH+]5CCN(C6=CC=C(N=N6)C7C(NC(CC7)=O)=O)CC5)=O)=CC=C1C#N.FC(C([O-])=O)(F)F
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
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How to Choose the Right Model Animal
Choosing the right model animal is a validity-driven decision in which the species, strain, sex, age, genetic background, disease-induction method, outcome measures, and welfare burden must match the scientific question rather than laboratory tradition or convenience. A model should be selected by judging face validity, construct validity, and predictive validity: whether it resembles the human phenotype, whether it reproduces relevant mechanisms, and whether results are likely to predict human biology or treatment response. Animal studies often fail to translate because of species differences, weak disease resemblance, poor experimental design, inadequate reporting, publication bias, and underuse of randomization, blinding, and sample-size justification. Unresolved questions include how to rank competing models objectively, how much human-disease complexity must be reproduced for a given objective, and when non-animal systems such as organoids, ex vivo tissue, or computational models
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
PROTAC AR Degrader-13 Related Classifications
HY-184195 Related Classifications
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