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Cat. No.: HY-178148

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AR antagonist 17

AR antagonist 17 is a selective, orally active, low brain-penetrant Androgen Receptor (AR) antagonist (IC₅₀ = 0.010 μM), effectively blocking AR dimerization and nuclear translocation, and demonstrating potent efficacy in several castration-resistant prostate cancer (CRPC) cells. AR antagonist 17 showed superior efficacy against variant drug-resistant AR mutants. AR antagonist 17 can inhibit tumor growth in an LNCaP xenograft model without apparent toxicity. AR antagonist 17 can be used for the study of castration-resistant prostate cancer (CRPC).

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CAS No.: 3064715-04-1
Formule: C₂₁H₂₀F₃N₃O₄S₂
Masse moléculaire:499.53

Stockage:

Please store the product under the recommended conditions in the Certificate of Analysis.

Data Sheet (275 KB)

AR antagonist 17 Chemical Structure

CAS No.: 3064715-04-1

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Activité biologique
- Description
- In Vitro
- In Vivo
Chemical Information
Pureté et documentation
Références
Calculators
Help & FAQs
Classifications
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Activité biologique

Description

In Vitro

AR antagonist 17 (Compound C13) shows excellent AR antagonistic activity and antiproliferative effects against AR-positive PCa cell lines (LNCaP (IC_{50_{= 1.02 μM), C4−2B (IC_{50_{= 3.86 μM), 22RV1 (IC_{50_{= 8.45 μM), and VCaP (IC_{50_{= 5.72 μM)), accompanied by low toxicity on normal cell lines 3T3 and Ges-1 (IC_{50_{> 20 μM)^[1].

AR antagonist 17 (0.2-2 μM, 2 weeks) completely inhibits clonal proliferation in LNCaP cells^[1].

AR antagonist 17 (0.02-2 μM, 48 h) dose-dependently suppresses the dihydrotestosterone (DHT)-induced transcriptional levels of prostate-specific antigen (PSA), and remarkably suppresses mRNA levels of two AR-regulated downstream genes, FKBP5 and TMPRSS2 in LNCaP cells^[1].

AR antagonist 17 (0.1-10 μM, 24 h) dose-dependently inhibits endogenous PSA protein expression but has no significant effect on AR protein expression in LNCaP cells^[1].

AR antagonist 17 (0.1-10 μM, 4 h) inhibits DHT-induced AR dimerization in a dose-dependent manner, and completely blocks this process at 10 μM in 293T cells^[1].

AR antagonist 17 (10 μM, 8 h) can cause AR to remain mainly in the cytoplasm and effectively prevent AR nuclear translocation in LNCaP cells^[1].

AR antagonist 17 demonstrates excellent antagonistic activity against these clinically prevalent AR resistance mutations, ARF877L/T878A (IC_{50_{= 0.35 μM), ARW742C (IC₅₀ = 0.50 μM), ARF877L (IC_{50_{= 0.070 μM)^[1].

AR antagonist 17 (2 μM, 48 h) significantly suppresses eight clinically relevant PCa recurrence markers: KLK3 (encoding PSA), TMPRSS2, KLK2, NKX3.1, SLC45A3, PMEPA1, TARP, and TM4SF1, alongside cancer-related processes, apoptosis regulators STK39, HERC3, and GRIN3A in LNCaP cells^[1].

AR antagonist 17 (2 μM, 48 h) significantly inhibits the expression of the pan-cancer-related biomarkers for DNA biosynthesis and repair, including EXO1, CYP11A1, PGC, RRM2, and FAM111B in LNCaP cells^[1].}}}}}}}}}}}}}}

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

Cell Proliferation Assay^[1]

Cell Line:

LNCaP cells
Concentration:

0.2 μM, 2 μM
Incubation Time:

2 week
Result:

Inhibited clonal proliferation at a concentration of 2.0 μM, showing better inhibitory activity against clonal proliferation than Enz 0.2 μM.

Western Blot Analysis^[1]

Cell Line:

LNCaP cells
Concentration:

0.1 Μm, 1 μM, 10 μM
Incubation Time:

24 h
Result:

Inhibited endogenous PSA protein expression but had no significant effect on AR protein expression in LNCaP cells.

RT-PCR^[1]

Cell Line:

LNCaP cells
Concentration:

0.02 μM, 0.2 μM, 2 μM
Incubation Time:

48 h
Result:

Suppressed the DHT-induced transcriptional levels of prostate-specific antigen (PSA), and remarkably suppressed mRNA levels of two AR-regulated downstream genes, FKBP5 and TMPRSS2.

Western Blot Analysis^[1]

Cell Line:

LNCaP cells
Concentration:

10 μM
Incubation Time:

8 h
Result:

Effectively inhibited DHT-induced AR nuclear translocation; AR mainly remains in the cytoplasm.

RT-PCR^[1]

Cell Line:

LNCaP cells
Concentration:

2 μM
Incubation Time:

48 h
Result:

Significantly suppressed eight clinically relevant PCa recurrence markers: KLK3 (encoding PSA), TMPRSS2, KLK2, NKX3.1, SLC45A3, PMEPA1, TARP, and TM4SF1, alongside cancer-related processes, apoptosis regulators STK39, HERC3, and GRIN3A in LNCaP cells.
Significantly inhibited the expression of the pan-cancer-related biomarkers for DNA biosynthesis and repair, including EXO1, CYP11A1, PGC, RRM2, and FAM111B in LNCaP cells.

In Vivo

AR antagonist 17 (5 mg/kg, oral gavage, 2-8 h) has low blood-brain barrier permeability in SD Rats, may have better safety and reduce central nervous system-related side effects^[1].
AR antagonist 17 (40 mg/kg, oral gavage, twice daily for 32 days) demonstrates significant tumor growth suppression throughout the treatment duration and does not induce significant body weight loss or other signs of toxicity during the experiment in CB17 SCID mice^[1].

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

Animal Model:

SD Rats^[1]
Dosage:

5.0 mg/kg
Administration:

Oral gavage
Result:

Had low blood-brain barrier permeability in SD Rats.

Animal Model:

LNCaP cells (1 × 107) were implanted subcutaneously into the right flanks of the 6-week-old male CB17 SCID mice^[1].
Dosage:

40 mg/kg
Administration:

Oral gavage, twice daily for 32 days
Result:

The tumor growth inhibition (TGI) of AR antagonist 17 was 123.41%.
Exhibited good tolerance and did not induce significant body weight loss or other signs of toxicity during the experiment.

Chemical Information

CAS No. 3064715-04-1
Masse moléculaire 499.53
Formule C₂₁H₂₀F₃N₃O₄S₂
SMILES

CC1=C(C=C(O1)C2=CC=CC(C(F)(F)F)=C2)C(NC3=NC(CN4CCS(=O)(CC4)=O)=CS3)=O
Livraison

Room temperature in continental US; may vary elsewhere.
Stockage

Please store the product under the recommended conditions in the Certificate of Analysis.

Pureté et documentation

Select Batch:

Pureté: 99.98%

Assay: 99.98%

ee.: 99.98%

Fiche technique (275 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Instruction de manipulation (2659 KB)

Références

[1]. Liao J, et al. Discovery of N-(thiazol-2-yl) Furanamide Derivatives as Potent Orally Efficacious AR Antagonists with Low BBB Permeability. J Med Chem. 2025 Sep 25;68(18):19688-19713. [Content Brief]

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Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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100 mg

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