Cat. No.: HY-124595

MPT0B098

MPT0B098 is a microtubule inhibitor with a K_i of 0.8 μM and an IC₅₀ of 0.8 μM. MPT0B098 inhibits tubulin polymerization, blocks HuR nuclear-cytoplasmic translocation to decrease HIF-1α mRNA stability, suppresses HIF-1α, TGF-β/Smad, JAK2/STAT3 and FAK/actin cytoskeleton signaling pathways, upregulates SOCS3 to reinforce the inhibition of JAK2/STAT3 cascade, and induces apoptosis. MPT0B098 can be used for research on multiple malignancies including head and neck squamous cell carcinoma and human non-small cell lung cancer.

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CAS No.: 1254363-89-7
화학식: C₂₀H₁₈N₂O₃S
분자량:366.44

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

MPT0B098 Chemical Structure

CAS No.: 1254363-89-7

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Biological Activity
- 제품 설명
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
순도&문서
References
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Biological Activity

제품 설명

IC₅₀ & Target^[1]

microtubule

0.8 μM (IC₅₀)

microtubule

0.8 μM (Ki)

HIF-1α

TGF-beta/Smad

JAK2

STAT3

All HIF/HIF Prolyl-Hydroxylase Isoforms :

All TGF-beta/Smad Isoforms :

Smad1
Smad3

All STAT Isoforms :

All JAK Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
HT-29	IC₅₀	87.5 nM Compound: 19	Antiproliferative activity against human HT-29 cells assessed as inhibition of cell growth after 72 hrs by methylene blue dye assay Antiproliferative activity against human HT-29 cells assessed as inhibition of cell growth after 72 hrs by methylene blue dye assay	10.1039/C0MD00052C
KB	IC₅₀	96 nM Compound: 19	Antiproliferative activity against human KB cells assessed as inhibition of cell growth after 72 hrs by methylene blue dye assay Antiproliferative activity against human KB cells assessed as inhibition of cell growth after 72 hrs by methylene blue dye assay	10.1039/C0MD00052C
MKN-45	IC₅₀	69.5 nM Compound: 19	Antiproliferative activity against human MKN45 cells assessed as inhibition of cell growth after 72 hrs by methylene blue dye assay Antiproliferative activity against human MKN45 cells assessed as inhibition of cell growth after 72 hrs by methylene blue dye assay	10.1039/C0MD00052C
NCI-H460	IC₅₀	101 nM Compound: 19	Antiproliferative activity against human H460 cells assessed as inhibition of cell growth after 72 hrs by methylene blue dye assay Antiproliferative activity against human H460 cells assessed as inhibition of cell growth after 72 hrs by methylene blue dye assay	10.1039/C0MD00052C

In Vitro

MPT0B098 inhibits proliferation of multiple human cancer cell lines, including H460, A549, H1299, HONE-1, PC-3, KB, HT29 and MKN-45 cells, with IC₅₀ values of 78-150 nM, while HUVEC cells are less sensitive to MPT0B098 with an IC₅₀ of 510 nM^[1].
MPT0B098 inhibits tubulin polymerization with a K_i of 0.8 μM, and with an IC₅₀ of 0.8 μM^[1].
MPT0B098 (0-1000 nM; 24 h) induces G₂/M phase arrest and apoptosis in A549 cells by increasing cyclin B1 and MPM2, changing Cdc25C and Cdc2 phosphorylation, increasing TUNEL-positive cells, promoting Bcl-2 phosphorylation and inducing PARP cleavage^[1].
MPT0B098 (0.2-0.5 μM; 16 h) inhibits VEGF-induced capillary-like tube formation in HUVECs^[1].
MPT0B098 (0.25 μM; 24 h) inhibits VEGF-induced HUVEC migration without reducing HUVEC viability^[1].
MPT0B098 (0-2 μM; 18 h) concentration-dependently reduces intracellular VEGF protein and secreted VEGF level in HUVECs; 0-0.9 μM MPT0B098 (18 h) suppresses hypoxia-induced VEGF secretion from A549 cells^[1].
MPT0B098 (0-0.9 μM; 18 h) decreases HIF-1α protein and produced stronger growth inhibition and higher caspase-3 activity under hypoxia, destabilizes HIF-1α mRNA, and reduces HuR nuclear-to-cytoplasmic translocation in A549 cells^[1].
MPT0B098 (111-444 nM; 72 h) suppresses proliferation of OEC-M1 cells under normoxia and hypoxia, with IC₅₀ of 222 nM under normoxia and IC₅₀ of 265 nM under hypoxia^[2].
MPT0B098 (111-444 nM; 18 h) dose-dependently downregulates HIF-1α protein, blocks hypoxia-triggered F-actin cytoskeleton rearrangement and reduces hypoxia-induced FAK phosphorylation without changing total FAK protein in hypoxic OEC-M1 cells^[2].
MPT0B098 (111-444 nM; 18-36 h) suppresses EMT transcription factors Twist and SNAI2/Slug in hypoxic OEC-M1 cells^[2].
MPT0B098 (111-444 nM; 36 h) downregulates vimentin and N-cadherin while partially restoring E-cadherin, suppresses TGF-β protein expression and Smad2/3 phosphorylation, and reduces TGF-β1 and TGF-β2 mRNA levels in hypoxic OEC-M1 cells^[2].
MPT0B098 (111-444 nM; 18 h pretreatment + TGF-β 18 h co-stimulation) reverses TGF-β-triggered Smad2/3 phosphorylation in hypoxic OEC-M1 cells^[2].
MPT0B098 (111 nM; 48 h) reverses hypoxia-induced mesenchymal morphological transformation of OEC-M1 cells^[2].
MPT0B098 (111 nM; 4-18 h) inhibits hypoxia-induced OEC-M1 cell migration in a time-dependent manner without obvious cytotoxicity^[2].
MPT0B098 (0.12-0.5 μM; 72 h) concentration-dependently suppresses viability of multiple OSCC cell lines (OEC-M1, HSC-3, SCC-25, Tu183, DOK, YD-15) with IC₅₀ of 0.14-0.45 μM, while normal HOK cells exhibit weak sensitivity with IC₅₀ of 6.3 μM^[3].
MPT0B098 (0.25 μM; 0-60 min) induces time-dependent tubulin depolymerization in OEC-M1 and HSC-3 cells, and microtubule network can partially recover after drug washout for 60 min^[3].
MPT0B098 (0.25, 0.5 μM; 12 h) triggers dose-dependent G₂/M cell cycle arrest and Annexin V-positive early apoptosis in OEC-M1 cells^[3].
MPT0B098 (0.12-1 μM; 24 h) elevates cleaved caspase-3 and PARP, and downregulates anti-apoptotic proteins Bcl-2, Mcl-1, Pim-1, Survivin in OSCC cells^[3].
MPT0B098 (0.25 μM; 15-240 min) gradually reduces phosphorylation and total protein levels of JAK2, TYK2 and STAT3 without altering STAT3 mRNA expression^[3].
MPT0B098 (0.25 μM; 0-60 min) selectively upregulates SOCS2 and SOCS3 protein levels rather than PIAS1/3 and SOCS1 in OSCC cells^[3].
MPT0B098 (0.25 μM) combined with 5 μM Cisplatin (HY-17394) or 5 μM 5-FU (HY-90006) produces markedly stronger proliferation inhibition and caspase-3 activation effects in OEC-M1 cells compared with single drug treatment^[3].

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

Cell Cycle Analysis^[1]

Cell Line:

A549
Concentration:

75, 150, 300, 450, 600 nM
Incubation Time:

24 h
Result:

Induced G₂/M phase arrest in a concentration-dependent manner.
Increased the G₂/M phase population with a concomitant loss of the G0/G1 phase, increased cyclin B1 and MPM2 levels, shifted Cdc25C phosphorylation status, and increased hypophosphorylated Cdc2.

Apoptosis Analysis^[1]

Cell Line:

A549
Concentration:

150, 300, 600 nM
Incubation Time:

24 h
Result:

Increased TUNEL-positive apoptotic cells in a concentration-dependent manner.
Increased the TUNEL-positive population from 1% in control cells to 4.9%, 24.7% and 78.7% at 150 nM, 300 nM and 600 nM, respectively.
Induced Bcl-2 phosphorylation and PARP cleavage.

Cell Migration Assay ^[1]

Cell Line:

HUVEC
Concentration:

0.25 μM
Incubation Time:

24 h
Result:

Inhibited VEGF-induced HUVEC migration without compromising HUVEC viability.

Apoptosis Analysis^[1]

Cell Line:

A549
Concentration:

0.1, 0.3, 0.6, 0.9, 1.2 μM
Incubation Time:

18 h
Result:

Reduced hypoxia-induced HIF-1α protein expression in a concentration-dependent manner.

Real Time qPCR^[1]

Cell Line:

A549
Concentration:

0.3, 0.6, 0.9 μM
Incubation Time:

24 h
Result:

Reduced HIF-1α mRNA levels under hypoxic conditions, whereas colchicine did not reduce HIF-1α mRNA levels under the same experimental condition.

Immunofluorescence^[1]

Cell Line:

A549
Concentration:

600 nM
Incubation Time:

6, 12, 18 h
Result:

Reduced cytoplasmic HuR distribution and decreased HIF-1α expression under hypoxic conditions.

Cell Proliferation Assay^[2]

Cell Line:

OEC-M1 under normoxic /hypoxic conditions
Concentration:

111, 222, 444 nM
Incubation Time:

72 h
Result:

Inhibited OEC-M1 cell proliferation under normoxic and hypoxic conditions, and exerted weaker hypoxia-induced drug resistance.

Western Blot Analysis^[2]

Cell Line:

OEC-M1
Concentration:

111, 222, 444 nM
Incubation Time:

18 h under hypoxia; 36 h under hypoxia; 18 h drug pretreatment + subsequent 18 h TGF-β co-stimulation under hypoxia
Result:

After 18 h hypoxic treatment, dose-dependently downregulated HIF-1α protein, blocked hypoxia-triggered F-actin cytoskeleton rearrangement and reduced hypoxia-induced FAK phosphorylation without changing total FAK protein levels.
After 18 h and 36 h hypoxic treatment respectively, suppressed EMT transcription factors Twist and SNAI2/Slug.
After 36 h hypoxic treatment, downregulated mesenchymal markers vimentin and N-cadherin, partially restored epithelial marker E-cadherin, decreased TGF-β protein expression and inhibited Smad2/3 phosphorylation.
After 18 h hypoxic drug pretreatment followed by another 18 h TGF-β co-stimulation under hypoxia, reversed TGF-β-triggered Smad2/3 phosphorylation in hypoxic OEC-M1 cells.

Real Time qPCR^[2]

Cell Line:

OEC-M1 under hypoxic conditions
Concentration:

111, 222, 444 nM
Incubation Time:

36 h
Result:

Decreased mRNA transcription levels of TGF-β1 and TGF-β2 in hypoxic OEC-M1 cells.

Immunofluorescence^[2]

Cell Line:

OEC-M1 under hypoxic conditions
Concentration:

111nM
Incubation Time:

48 h
Result:

Reversed hypoxia-induced mesenchymal fibroblast-like morphological transformation of OEC-M1 cells.

Cell Migration Assay ^[2]

Cell Line:

OEC-M1 under hypoxic conditions
Concentration:

4 h, 6 h, 8 h, 18 h
Incubation Time:

48 h
Result:

Time-dependently inhibited hypoxia-induced OEC-M1 cell migration without obvious cytotoxicity, and its anti-migration activity was superior.

Cell Cycle Analysis^[2]

Cell Line:

OEC-M1
Concentration:

0.25 μM, 0.5 μM
Incubation Time:

12 h
Result:

Induced dose-dependent G₂/M phase cell cycle arrest in OEC-M1 cells.

Apoptosis Analysis^[3]

Cell Line:

OEC-M1, HSC-3, DOK, YD-15
Concentration:

0.12 μM, 0.25 μM, 0.5 μM, 1 mM
Incubation Time:

24 h
Result:

Induced concentration-dependent cell apoptosis.
Elevated activated caspase-3 and cleaved PARP.
Downregulated anti-apoptotic proteins including Bcl-2, Mcl-1, Pim-1 and Survivin.

Western Blot Analysis^[3]

Cell Line:

OEC-M1, HSC-3
Concentration:

0.25 μM
Incubation Time:

15 min, 30 min, 60 min, 120 min, 240 min
Result:

Time-dependently decreased phosphorylation and total protein levels of JAK2, TYK2 and STAT3 without altering STAT3 MRNA.
Selectively upregulated SOCS2 and SOCS3 protein while SOCS1, PIAS1 and PIAS3 kept stable expression.
Prolonged the half-life of SOCS3 protein, strengthened the binding between SOCS3 and JAK2/TYK2, and promoted the ubiquitination and degradation of JAK2 and TYK2.

Cell Cytotoxicity Assay^[3]

Cell Line:

OEC-M1
Concentration:

0.25 μM
Incubation Time:

24 h, 48 h, 72 h
Result:

The combination with 5μM cisplatin (HY-17394) or 5μM 5-FU (HY-90006) produced stronger growth inhibition and higher caspase-3 activity.

Western Blot Analysis^[3]

Cell Line:

OEC-M1, HSC-3
Concentration:

0.25 μM
Incubation Time:

24 h co-culture with IL-6
Result:

Suppressed IL-6-induced JAK2/STAT3 phosphorylation and reversed IL-6-mediated apoptosis inhibition of oral cancer cells.

Cell Viability Assay^[3]

Cell Line:

Plasmid/shRNA transfected for 48 h in OEC-M1, HSC-3, DOK, YD-15
Concentration:

0.25 μM
Incubation Time:

24 h
Result:

SOCS3 overexpression enhanced MPT0B098-triggered caspase-3 activity, while SOCS3 knockdown weakened the pro-apoptotic effect; STAT3 silencing sensitized OSCC cells to cytotoxicity.

In Vivo

MPT0B098 (25, 50 mg/kg; i.p.; once daily; for 5 consecutive days) suppresses tumor growth and reduces microvessel density in A549 human non-small cell lung cancer xenograft nude mouse model^[1].

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

Animal Model:

Five-week-old nude mice subcutaneously implanted with A549 cells (2 × 10⁶ cells) into the right flank region^[1]
Dosage:

25, 50 mg/kg
Administration:

Intraperitoneal injection (i.p.); once daily; for 5 consecutive days
Result:

Intraperitoneal injection (i.p.); once daily; for 5 consecutive days Delayed A549 xenograft tumor growth in a dose-dependent manner.
Reduced CD31-positive microvessel density in tumor specimens.
Was well tolerated up to 50 mg/kg.
Caused no obvious signs of toxicity in drug-treated mice.
Maintained body weight loss within 15% in all treatment groups.

Chemical Information

CAS No. 1254363-89-7
분자량 366.44
화학식 C₂₀H₁₈N₂O₃S
SMILES

O=S(=O)(C1=CC=C(OC)C=C1)N2C3=C(C=CC=C3CC2)C=4C=CN=CC4
선적

Room temperature in continental US; may vary elsewhere.
보관

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

순도&문서

Handling Instructions (2659 KB)

References

[1]. Cheng YC, et al. MPT0B098, a novel microtubule inhibitor that destabilizes the hypoxia-inducible factor-1α mRNA through decreasing nuclear-cytoplasmic translocation of RNA-binding protein HuR. Mol Cancer Ther. 2013;12(7):1202-1212. [Content Brief]

[2]. Tsai IT, et al. Novel microtubule inhibitor MPT0B098 inhibits hypoxia-induced epithelial-to-mesenchymal transition in head and neck squamous cell carcinoma. J Biomed Sci. 2018;25:28. PMID: 29592811. DOI: 10.1186/s12929-018-0432-6. [Content Brief]

[3]. Peng HY, et al. MPT0B098, a microtubule inhibitor, suppresses JAK2/STAT3 signaling pathway through modulation of SOCS3 stability in oral squamous cell carcinoma. PLoS One. 2016;11(7):e0158440. PMID: 27367272. DOI: 10.1371/journal.pone.0158440. [Content Brief]

Calculators

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Help & FAQs

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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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MPT0B098

All HIF/HIF Prolyl-Hydroxylase Isoforms

All TGF-beta/Smad Isoforms

All STAT Isoforms

All JAK Isoforms

Biological Activity

Chemical Information

순도&문서

References

Calculators

Help & FAQs

MPT0B098 Related Classifications

HY-124595 Related Classifications