1. Vitamin D Related/Nuclear Receptor Apoptosis PI3K/Akt/mTOR MAPK/ERK Pathway Stem Cell/Wnt
  2. Androgen Receptor c-Myc Akt mTOR ERK PDK-1 PI3K Apoptosis
  3. WH23

WH23 is a dehydrogenase/reductase SDR family member 11 (DHRS11) inhibitor with IC50 values of 0.037 μM. WH23 binds to DHRS11, forming a hydrogen bond with the enzyme’s His210 residue. WH23 suppresses androgen receptor mRNA and protein expression, reduces c-Myc expression, and inhibits cancer cell proliferation. WH23 inhibits PI3K/AKT signaling by reducing phosphorylation of PDK1, AKT, mTOR, and ERK. WH23 enhances Capivasertib (HY-15431)-induced cytotoxicity and apoptosis. WH23 can be used for the research of luminal androgen receptor-positive triple-negative breast cancer.

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

WH23

WH23 Chemical Structure

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Description

WH23 is a dehydrogenase/reductase SDR family member 11 (DHRS11) inhibitor with IC50 values of 0.037 μM. WH23 binds to DHRS11, forming a hydrogen bond with the enzyme’s His210 residue. WH23 suppresses androgen receptor mRNA and protein expression, reduces c-Myc expression, and inhibits cancer cell proliferation. WH23 inhibits PI3K/AKT signaling by reducing phosphorylation of PDK1, AKT, mTOR, and ERK. WH23 enhances Capivasertib (HY-15431)-induced cytotoxicity and apoptosis. WH23 can be used for the research of luminal androgen receptor-positive triple-negative breast cancer[1].

In Vitro

WH23 (Compound WH23) potently inhibits wild-type DHRS11 with an IC50 of 0.037 ± 0.0079 μM, and its binding relies heavily on hydrogen bonding with His210 of DHRS11, as evidenced by a 24-fold loss of potency against the His210Ala mutant (IC50 = 0.87 μM)[1].
WH23 inhibit CBR1 with an IC50 of 1.7 nM and exhibits 46-fold selectivity for DHRS1[1] .
WH23 (10 μM; 2-72 h) suppresses androgen signaling and proliferation in MDA-MB-453 cells by reducing AR mRNA and protein levels, inhibiting 11KAdione (HY-135794)-induced c-Myc expression, and blocking androgen-driven cell growth[1].
WH23 (10 μM; 0.5-3 h) inhibits PI3K/AKT and MAPK signaling in MDA-MB-453 cells by reducing phosphorylation of key pathway proteins including PDK1, AKT, mTOR, and ERK[1].
WH23 (5-20 μM; 48 h) selectively reduces viability of AR-positive MDA-MB-453 triple-negative breast cancer cells, with minimal effect on AR-negative MDA-MB-231 cells[1].
WH23 (2-10 μM; 48 h) synergistically enhances Capivasertib (HY-15431)-induced cytotoxicity and apoptosis in Capivasertib-resistant MDA-MB-453 cells, with combination index values less than 1 confirming synergism[1].

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

Western Blot Analysis[1]

Cell Line: MDA-MB-453 cells
Concentration: 10 μM
Incubation Time: 0.5, 1, or 3 h
Result: Reduced phosphorylation of ERK (MAPK pathway), and decreased phosphorylation of PDK1, AKT, and mTOR (PI3K/AKT pathway).

Cell Viability Assay[1]

Cell Line: MDA-MB-453 (AR-positive, LAR subtype) and MDA-MB-231 (AR-negative, non-LAR subtype) triple-negative breast cancer cells
Concentration: 5, 10, 20 μM
Incubation Time: 48 h
Result: Significantly reduced viability of MDA-MB-453 cells at concentrations of 5, 10, 15, and 20 μM, but had minimal impact on viability of MDA-MB-231 cells.
Molecular Weight

326.30

Formula

C18H14O6

SMILES

O=C1C=C(/C=C/C2=CC=C(O)C=C2O)OC3=C(C)C(O)=CC(O)=C13

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Room temperature in continental US; may vary elsewhere.

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

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  • 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.

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WH23
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HY-181670
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