2. JAK/STAT Signaling Apoptosis PI3K/Akt/mTOR Epigenetics Protein Tyrosine Kinase/RTK Stem Cell/Wnt
  3. Pim Apoptosis AMPK DYRK STAT MDM-2/p53
  4. VS-II-173

VS-II-173 is a pan-Pim kinase inhibitor with IC50 values ​​of 0.07 μM and 0.02 μM for Pim1 and Pim3, respectively, and a residual activity of 46% for Pim2 at 1 μM. VS-II-173 also inhibits kinases such as HIPK2, PRK2, RSK1, DYRK1a and AMPKα1, selectively inhibiting acute myeloid leukemia (AML) cells with significantly lower toxicity to non-malignant cells (EC50 > 30 μM). VS-II-173 weakens the phosphorylation of substrates such as Stat5 (Y694), MDM2 (S166), Bad (S112), and 4E-BP1 (T37/46) by inhibiting Pim kinase-mediated signaling pathways, blocking pro-survival signals in AML cells and inducing apoptosis. VS-II-173 synergistically enhances anti-AML activity when combined with Daunorubicin (HY-13062A). VS-II-173 can be used in AML research, especially for AML with FLT3-ITD mutations and NPM1 mutations .

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

VS-II-173

VS-II-173 Chemical Structure

CAS No. : 1627962-21-3

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VS-II-173 Related Antibodies

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PIM1 PIM2 PIM3

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NUAK1 NUAK2 AMPK AMPK α1β1γ1 AMPK α2β1γ1 AMPK α1β2γ1 AMPK α2β2γ1 BRSK1 BRSK2 HUNK AMPKα

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DYRK1 DYRK2 DYRK3 DYRK4 HIPK PRP4

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STAT3 STAT5 STAT6 STAT1

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Description

VS-II-173 is a pan-Pim kinase inhibitor with IC50 values ​​of 0.07 μM and 0.02 μM for Pim1 and Pim3, respectively, and a residual activity of 46% for Pim2 at 1 μM. VS-II-173 also inhibits kinases such as HIPK2, PRK2, RSK1, DYRK1a and AMPKα1, selectively inhibiting acute myeloid leukemia (AML) cells with significantly lower toxicity to non-malignant cells (EC50 > 30 μM). VS-II-173 weakens the phosphorylation of substrates such as Stat5 (Y694), MDM2 (S166), Bad (S112), and 4E-BP1 (T37/46) by inhibiting Pim kinase-mediated signaling pathways, blocking pro-survival signals in AML cells and inducing apoptosis. VS-II-173 synergistically enhances anti-AML activity when combined with Daunorubicin (HY-13062A). VS-II-173 can be used in AML research, especially for AML with FLT3-ITD mutations and NPM1 mutations [1][2].

IC50 & Target

PIM1

0.07 μM (IC50)

PIM2

~1 μM ()

PIM3

0.02 μM (IC50)

DYRK1

 

AMPK

 

In Vitro

VS-II-173 (1 μM) inhibits a range of protein kinases beyond Pim kinases, with potent activity against DYRK1A, HIPK2, PRK2, RSK1, and AMPKa1[1].
VS-II-173 (1 μM; 24 h) synergizes with Daunorubicin to induce cell death in Molm-13 AML cells, with additive effects with Etoposide (HY-13629), Emetine, Geldanamycin (HY-15230), and antagonism with high-concentration Bortezomib (HY-10227)[1].
VS-II-173 (3-12 μM; 1-6 h) modulates cell signaling in AML cell lines by downregulating Pim kinases and dephosphorylating Stat5, Bad, 4E-BP1, and MDM2[1].
VS-II-173 (EC50=3.7 μM，72 h) induces apoptosis in MOLM-13 acute myeloid leukemia cells[2].
VS-II-173 shows low cytotoxicity toward Normal Rat Kidney (NRK) epithelial cells (EC50 =>30 μM, 72 h)[2].

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

VS-II-173 Related Antibodies

Western Blot Analysis[1]

Cell Line: human AML cell lines (Molm-13, MV4-11, OCI-AML3)
Concentration: 3, 6, 12 μM
Incubation Time: 1, 3, 6 h
Result: Induced transient downregulation of Pim1, Pim2, and Pim3 in Molm-13 cells; dephosphorylated Stat5 in Molm-13 and MV4-11 cells; reduced phospho-Bad in MV4-11 cells; and decreased p-4E-BP1 and pMDM2 in OCI-AML3 cells.
Molecular Weight

264.24

Formula

C14H8N4O2
CAS No.
SMILES

O=[N+]([O-])C1=C(N=CC2=C3C=CC=C2)C3=C4C=NNC4=C1
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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VS-II-173 Related Classifications

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Keywords:

VS-II-1731627962-21-3PimApoptosisAMPKDYRKSTATMDM-2/p53Pim kinasesAMP-activated protein kinaseDual specificity tyrosine phosphorylation regulated kinaseDual specificity tyrosine regulated kinaseapoptosisStat5MDM2 phosphorylationFLT3-ITD mutationsAML cell survival signalingAML blastsacute myeloid leukemiaPim-1AML cell deathPim kinaseInhibitorinhibitorinhibit

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