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Fig. 1 · Structure
Cat. No.
A10982
CAS No.
745833-23-2
Alternate CAS
479543-46-9
Formula
C19H12F4N4O2
Mol. Weight
404.3

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VX-702

Cat. No. A10982 CAS 745833-23-2

p38 MAPK inhibitor

VX-702 is an orally bioavailable inhibitor of p38 MAP kinase that inhibits platelet agonist induced p38 activation (IC50= 4 to 20 nM).

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Publications for VX-702

1 publication citing this product
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Biological Activity

Bioactivity / Mechanism

VX-702 reduced IL-1β-induced IFNAR1 priming phosphorylation in HeLa cells, consistent with inhibition of p38-dependent signaling. Direct kinase experiments also showed inhibition of NLK-mediated phosphorylation, so VX-702 should not be interpreted as an exclusively p38-directed probe. [1,2]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

In Vitro Studies

In 1205Lu melanoma cells, 1 μM VX-702 pretreatment increased growth inhibition during a subsequent 72-hour IFNα exposure. This result describes a combination response in a defined cell model; it does not establish a single-agent cytotoxic potency. [1]

IL-1β-induced IFNAR1 phosphorylation in HeLa cells

Cell-based study · HeLa cells stimulated with IL-1β [1]

VX-702 reduced IL-1β-induced IFNAR1 Ser532 priming phosphorylation in an immunoprecipitation/immunoblot comparison. Total IFNAR1 was measured. DMSO, SB203580, SP600125 and NBD comparisons support a p38-pathway interpretation, without proving target exclusivity.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
IL-1β-induced IFNAR1 Ser532 phosphorylation relative to total immunoprecipitated IFNAR1qualitative response Reduced with VX-702 relative to IL-1β plus DMSO[1]

Literature-Reported Treatment Conditions

Treatment concentration
1 μg/mL
Exposure duration
Pretreatment duration not specified for Figure 4C; IL-1β stimulation for 30 min
Method
VX-702 pretreatment followed by IL-1β (5 ng/mL); IFNAR1 IP/IB
Vehicle
DMSO control
Co-treatment
IL-1β stimulus, 5 ng/mL
Reported limits
VX-702 pretreatment time, lot/purity and replicate count for panel C are not specified in the acquired caption/main methods; supplement not retrieved.
Methods and source locations

Compound reported in the paper: VX-702; Compound label in the paper: VX-702

Evidence for the paper’s named VX-702 material; no supplier or Adooq lot validation, salt conversion, or clinical efficacy inference.

Figure 4C and caption; Results paragraph on priming phosphorylation; Methods Antibodies and Immunotechniques

IL-1β-induced IFNAR1 Ser532 phosphorylation relative to total immunoprecipitated IFNAR1: IFNAR1 immunoprecipitation followed by phospho-Ser532 and total IFNAR1 immunoblotting — Figure 4C image and caption; Results priming-phosphorylation paragraph

VX-702 and IFNα response in 1205Lu melanoma cells

Cell-based study · 1205Lu human melanoma cells [1]

VX-702 pretreatment increased IFNα-associated growth inhibition; the figure marks P < 0.05 at the highest plotted IFNα concentration. This is a combination response in one melanoma line, not a VX-702 IC50 or evidence of broad single-agent cytotoxicity.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Growth inhibition during IFNα exposure with versus without VX-702 pretreatmentqualitative response Greater inhibition with VX-702; P < 0.05 marked at 40 IU/mL IFNα; mean ± SD from 3 independent experiments, each in triplicate[1]

Literature-Reported Treatment Conditions

Treatment concentration
1 μM
Exposure duration
1 h pretreatment; then 72 h IFNα treatment
Method
Proliferation assessed with CellTiter 96 Non-Radioactive Cell proliferation Assay
Vehicle
Comparator labeled vehicle in Figure 7D; composition not specified for this panel
Co-treatment
IFNα: 0, 20 and 40 IU/mL plotted in Figure 7D
Reported limits
VX-702 lot/purity and vehicle composition for this panel not specified in acquired main text; no IC50 reported for this design.
Methods and source locations

Compound reported in the paper: VX-702; Compound label in the paper: VX-702

Evidence for the paper’s named VX-702 material; no supplier or Adooq lot validation, salt conversion, or clinical efficacy inference.

Figure 7D and caption; Results final paragraph; Methods Cell lines and cancer samples

Growth inhibition during IFNα exposure with versus without VX-702 pretreatment: CellTiter 96 proliferation assay; no numerical effect size interpolated from curves — Figure 7D image/caption; Methods Cell lines and cancer samples

VX-702 inhibition of immunopurified NLK catalytic activity

Biochemical assay · V5-tagged NLK immunoprecipitated from MCF7 cells, with myelin basic protein (MBP) substrate [2]

The VX-702 dose series reduced MBP phosphorylation and NLK autophosphorylation. Anti-V5/no-drug and IgG IP controls and a protein-loading panel are shown. This directly supports NLK activity as a relevant additional target; it does not establish a numeric NLK IC50 or exclusive p38 inhibition.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
MBP phosphorylation and NLK autophosphorylation by immunopurified V5-NLKqualitative response Both signals decreased across the VX-702 concentration series; qualitative blot result[2]

Literature-Reported Treatment Conditions

Treatment concentration
0.05, 0.5 and 5 μM (Figure 2D labels)
Method
V5-NLK immunoprecipitation and in vitro kinase assay with MBP; VX-702 maintained during the kinase assay
Reported limits
Panel D-specific exposure/reaction duration and vehicle composition not established from acquired text. Supplement-1 contents not retrieved; ERα/SRC-3 reaction conditions are not borrowed for MBP.
Methods and source locations

Compound reported in the paper: VX-702; Compound label in the paper: VX-702

Evidence for the paper’s named VX-702 material; no supplier or Adooq lot validation, salt conversion, or clinical efficacy inference.

Figure 2D and caption; Results Identification of a selective dual p38 and NLK inhibitor; Methods Cell viability assays (material source)

MBP phosphorylation and NLK autophosphorylation by immunopurified V5-NLK: In vitro kinase assay with MBP and NLK IP; IgG IP and no-drug controls; total NLK protein shown — Figure 2D image and caption; Results dual-inhibitor identification

In Vivo Studies

In bleomycin-treated wild-type mice, oral VX-702 at 10 mg/kg daily from day 9 through day 21 reduced lung collagen burden and histological fibrosis at day 21. This was treatment during fibrogenesis, before peak fibrosis. [3]

In mice with inducible fibroblast-specific MKP1 deficiency, VX-702 at 10 mg/kg daily from day 21 to day 56 reduced persistent lung fibrosis relative to vehicle. The genetic model and the possibility of effects in other cell types limit attribution of the response solely to fibroblast p38. [3]

VX-702 during pulmonary fibrogenesis in wild-type mice

Animal study · Wild-type C57BL/6 male and female mice; WT animals obtained at 8–10 weeks of age; bleomycin-induced pulmonary fibrosis [3]

Daily VX-702 during days 9–21 reduced lung hydroxyproline and histological fibrosis at day 21 relative to bleomycin plus vehicle. Treatment begins after injury and before peak fibrosis. This design does not test reversal of established fibrosis in otherwise unmodified animals.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Lung hydroxyproline content at day 21 and histological fibrosisqualitative response Lower hydroxyproline with VX-702 versus bleomycin plus vehicle (P < 0.05, Figure 6B); less severe trichrome-stained fibrosis[3]

Conditions shared by the study groups

Route
Oral gavage
Frequency
Daily
Treatment course
Day 9 through day 21 after bleomycin; harvest day 21
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Bleomycin plus VX-702
10 mg/kg VX-702		Bleomycin plus vehicle; saline reference group also shownReduced hydroxyproline and less histological fibrosis relative to bleomycin plus vehicle[3]
Bleomycin plus VX-702
Model: Wild-type C57BL/6 male and female mice; WT animals obtained at 8–10 weeks of age; bleomycin-induced pulmonary fibrosis
Reported limits: Vehicle formulation and exact group n not transcribed from acquired legible source.
Methods and source locations

Compound reported in the paper: VX-702; Compound label in the paper: VX-702

Evidence for the paper’s named VX-702 material; no supplier or Adooq lot validation, salt conversion, or clinical efficacy inference.

Figure 6A-C and caption; Results paragraph beginning Having identified; Methods Animal studies and Statistics

Lung hydroxyproline content at day 21 and histological fibrosis: Hydroxyproline in pooled left and right upper/middle lobes; representative Masson’s trichrome in right lower lobe; mean ± SEM; 1-way ANOVA with Tukey multiple-comparison test — Figure 6B-C images and caption; Methods Animal studies and Statistics

Bleomycin plus VX-702 · Figure 6A-C and caption; Results paragraph beginning Having identified; Methods Animal studies and Statistics

VX-702 after peak fibrosis in fibroblast-specific MKP1-deficient mice

Animal study · Bleomycin-treated Col1a2CreERT2 Dusp1fl/fl (Cre+) mice and Cre− Dusp1fl/fl controls; tamoxifen-induced fibroblast-specific MKP1 deletion starting day 21 [3]

VX-702 from day 21 to day 56 reduced persistent collagen burden in Cre+ mice, toward that in spontaneously resolving Cre− controls. Histology supported the response. The genetic deficiency and simultaneous tamoxifen induction constrain generalization; actions in other cell types cannot be excluded.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Lung hydroxyproline and histology at day 56 following post-peak treatmentqualitative response Lower hydroxyproline in VX-702-treated Cre+ mice versus Cre+ vehicle (P < 0.01, Figure 6E); reduced persistent histological fibrosis[3]

Conditions shared by the study groups

Route
Oral gavage
Frequency
Daily
Treatment course
Day 21 through day 56; harvest day 56
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Cre+ bleomycin plus VX-702
10 mg/kg VX-702		Cre+ bleomycin plus vehicle and Cre− bleomycin controlsReduced persistent hydroxyproline burden and histological fibrosis[3]
Cre+ bleomycin plus VX-702
Model: Bleomycin-treated Col1a2CreERT2 Dusp1fl/fl (Cre+) mice and Cre− Dusp1fl/fl controls; tamoxifen-induced fibroblast-specific MKP1 deletion starting day 21
Reported limits: Vehicle formulation and exact group n not transcribed from acquired legible source. Tamoxifen diet starts on day 21 in the resolution protocol.
Methods and source locations

Compound reported in the paper: VX-702; Compound label in the paper: VX-702

Evidence for the paper’s named VX-702 material; no supplier or Adooq lot validation, salt conversion, or clinical efficacy inference.

Figure 6D-G and caption; Results resolution paragraph; Methods Animal studies and Statistics

Lung hydroxyproline and histology at day 56 following post-peak treatment: Hydroxyproline assay and representative Masson’s trichrome histology; individual mice plotted; mean ± SEM; 1-way ANOVA with Tukey multiple-comparison test — Figure 6D-F image and caption; Methods Animal studies and Statistics

Cre+ bleomycin plus VX-702 · Figure 6D-G and caption; Results resolution paragraph; Methods Animal studies and Statistics

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 745833-23-2
Alternate CAS 479543-46-9
Applications p38 MAPK inhibitor
Formula C19H12F4N4O2
Molecular Weight 404.3
SMILES
C1=CC(=C(C(=C1)F)N(C2=NC(=C(C=C2)C(=O)N)C3=C(C=C(C=C3)F)F)C(=O)N)F

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 77 mg/mL (190.45 mM)
Water Insoluble
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
28 mg/mL
Vehicle
30% PEG400+0.5% Tween80+5% propylene glycol

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Huangfu WC, Qian J, Liu C, et al. Inflammatory signaling compromises cell responses to interferon alpha. Oncogene (2012). PMID: 21666722 DOI: 10.1038/onc.2011.221 Source material
  2. [2] Wang X, Veeraraghavan J, Liu CC, et al. Therapeutic Targeting of Nemo-like Kinase in Primary and Acquired Endocrine-resistant Breast Cancer. Clin Cancer Res (2021). PMID: 33542078 DOI: 10.1158/1078-0432.ccr-20-2961 Source material
  3. [3] Fortier SM, Walker NM, Penke LR, et al. MAPK phosphatase 1 inhibition of p38α within lung myofibroblasts is essential for spontaneous fibrosis resolution. J Clin Invest (2024). PMID: 38512415 DOI: 10.1172/jci172826 Source material

Publications

1 publication citing this product

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