Art. -Nr.: HY-13919

Napabucasin

Name: Napabucasin
Brand: MedChemExpress
SKU: HY-13919
Price: 77.00 USD
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(Synonyms: BBI608; BB608)

29 Cited Publications

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Based on 29 publication(s) in Google Scholar

Napabucasin (BBI608; BB608) is an orally active STAT3 inhibitor. Napabucasin inhibits STAT3/RelA signaling and induces cancer cell apoptosis, cell cycle arrest, and ROS/DNA damage, inhibiting cancer cell proliferation, migration, and invasion. Napabucasin, upon activation by NQO1/POR, enhances Docetaxel (HY-B0011) sensitivity and inhibits BCR-ABL1-positive leukemia self-renewal. Napabucasin recruits cytotoxic T/B lymphocytes, enhances immune checkpoint blockade, prevents liver metastasis, and radiosensitizes diffuse midline glioma. Napabucasin can be used in research on cancers such as glioblastoma, pancreatic ductal adenocarcinoma, and prostate cancer.

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Reinheit : 99.94%
CAS. Nr.: 83280-65-3
Formel: C₁₄H₈O₄
Molecular Weight:240.21

Speicherung:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 2 years , -20°C, 1 year

Napabucasin Chemical Structure

CAS. Nr.: 83280-65-3

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Use of MCE Products

Fluorescent Dye

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

Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
- Clinical Trial
Chemical Information
Publications (29)
Lösungsmittel & Löslichkeit
- In Vitro
- In Vivo
Reinheit & Dokumentation
Verweise
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

IC₅₀ & Target

STAT3

Alle STAT Isoform-spezifische Produkte anzeigen :

Alle NF-κB Isoform-spezifische Produkte anzeigen :

Cellular Effect

Cell Line	Type	Value	Description	References
U-87MG ATCC	IC50	6.4 μM	Antiproliferative activity against human U87MG GBM cells assessed as viability reduction incubated 24, 48, and 72 hrs by CCK-8 assay. Antiproliferative activity against human U87MG GBM cells assessed as viability reduction incubated 24, 48, and 72 hrs by CCK-8 assay.	31277685
LN-229	IC50	5.6 μM	Antiproliferative activity against human LN229 GBM cells assessed as viability reduction incubated 24, 48, and 72 hrs by CCK-8 assay. Antiproliferative activity against human LN229 GBM cells assessed as viability reduction incubated 24, 48, and 72 hrs by CCK-8 assay.	31277685
PC-3	IC50	3.67 μM	Inhibition of viability in human PC-3 prostate cancer bulk cells by napabucasin with IC₅₀ determined by cell viability assay. Inhibition of viability in human PC-3 prostate cancer bulk cells by napabucasin with IC₅₀ determined by cell viability assay.	26899963
PC-3	IC50	1.35 μM	Inhibition of viability in human PC-3 prostate cancer stem cells by napabucasin with IC₅₀ determined by cell viability assay. Inhibition of viability in human PC-3 prostate cancer stem cells by napabucasin with IC₅₀ determined by cell viability assay.	26899963
A549/CDDP	IC50	0.19 μM	Antiproliferative activity against human chemoresistant A549/DDP NSCLC cells assessed as viability reduction after 48 hrs by CCK-8 assay. Antiproliferative activity against human chemoresistant A549/DDP NSCLC cells assessed as viability reduction after 48 hrs by CCK-8 assay.	37748583

In Vitro

Anti-cancerApoptosisCell Cycle RegulationCytokines & ChemokinesOxidative StressOthers

Anti-cancer

Napabucasin (1-10 μM; 24-72 h) inhibits U87MG and LN229 GBM cell viability with IC₅₀ values of 6.4 and 5.6 μM, respectively^[1].
Napabucasin (5 μM; 48 h) reduces EdU incorporation in U87MG and LN229 cells^[1].
Napabucasin (5 μM; 10 d) inhibits colony formation in U87MG and LN229 cells^[1].
Napabucasin (1 μM; 1 d) attenuates wound healing in U87MG and LN229 cells^[1].
Napabucasin (1 μM; 24 h) reduces the invasive ability of U87MG and LN229 cells through Matrigel and decreases MMP2/MMP9 protein levels^[1].
Napabucasin (1 μM; 48 h) inhibits the invasive ability of U87MG and LN229 cells in a 3D spheroid environment^[1].
Napabucasin (1-10 μM; 48 h) reduces STAT3 protein levels in U87MG and LN229 cells in a dose-dependent manner^[1].
Napabucasin (5 μM; 10 d) inhibits the self-renewal and sphere formation of U87MG-GSCs and LN229-GSCs^[1].
Napabucasin (5 μM; 10 d) downregulates the mRNA of STAT3 and stemness-related genes in U87MG-GSCs and LN229-GSCs^[1].
Napabucasin (5 μM; 10 d) reduces STAT3, β-catenin, and c-Myc protein levels in U87MG-GSCs and LN229-GSCs^[1].
Napabucasin (0.5 µM; 6 h) induces NQO1-dependent γH2AX DNA damage in MiaPaCa2 Rosa26 cells, but not in NQO1-71 or NQO1-163 clones^[2].
Napabucasin (1 μM; 48-120 h) inhibits the proliferation of PC-3 and 22RV1 prostate cancer cells^[3].
Napabucasin (1 μM; 24 h) inhibits colony formation in PC-3 and 22RV1 prostate cancer cells^[3].
Napabucasin (18 h) reduces the migration of PC-3 and 22RV1 prostate cancer cells^[3].
Napabucasin (1 μM; 48 h) increases the sensitivity of PC-3 to docetaxel, reducing the docetaxel IC₅₀ from 22.269 nM to 9.516 nM^[3].
Napabucasin (1 μM; 24 h) reduces stemness-high cancer cells by 10-fold and 7-fold in PC-3 and 22RV1 sphere cultures, respectively^[3].
Napabucasin inhibits side population cells of 22RV1 prostate cancer cells^[3].
Napabucasin inhibits CD133+/CD44+ prostate cancer stem-like cells in PC-3^[3].
Napabucasin inhibits PrCSC sphere formation enriched from PC-3 and 22RV1^[3].
Napabucasin shows lower IC₅₀ values in 22RV1 and PC-3 cancer stem cells (1.043 and 1.35 μM) than in bulk cancer cells (1.57 and 3.67 μM)^[3].
Napabucasin (0-2 μM; 24 h) dose-dependently downregulates β-catenin, KLF-4, NANOG, Survivin, and C-myc protein expression in PC-3-derived PrCSCs^[3].
Napabucasin downregulates the mRNA expression of Nanog, Klf4, survivin, and β-catenin in PC-3 high-stemness cancer cells^[3].
Napabucasin (0.17-1.01 μM; 48 h) inhibits the proliferation of NSCLC cell lines, including the chemotherapy-resistant A549/DDP and A549/GEM cells, with IC₅₀ values of 0.19 μM and 0.17 μM, respectively^[4].
Napabucasin (0.2-0.4 μM; 2 weeks) inhibits colony formation of NSCLC cells^[4].
Napabucasin (0.2 μM; 24 h) partially inhibits the migration of A549 and H1975 cells^[4].
Napabucasin (0.2 μM; 48 h) reduces CD44+ cells to 2% in A549/DDP and A549/GEM chemoresistant NSCLC cells and decreases SP cells^[4].
Napabucasin (0.2 μM; 48 h) inhibits the expression of p-STAT3, β-catenin, and SOX-2 in A549/DDP cells^[4].
Napabucasin (2 µM; 72 h) inhibits secondary colony formation after serial replating of CD34+CD38-CD19+ cells derived from T315I BCR-ABL1 and WT-BCR-ABL1^[6].
Napabucasin (72 h) is a potent in vitro cytotoxic agent in DMG cultures, with IC₅₀ values of 0.80, 1.05, 0.84, and 1.44 µM in DIPG36, DIPG6, DIPG17, and SF8628 cells, respectively^[7].
Napabucasin (0.2 µM; 14 days) radiosensitizes DIPG36 and DIPG-KAPP cells, with Bliss synergy scores of 16.7 and 17.36, respectively^[7].

Anti-cancer

Apoptosis

Napabucasin (5 μM; 48 h) induces apoptosis in U87MG and LN229 cells^[1].
Napabucasin (5 μM; 48 h) increases cleaved caspase-3 immunofluorescence in U87MG and LN229 cells^[1].
Napabucasin (5 μM; 48 h) reduces STAT3 expression in U87MG and LN229 cells^[1].
Napabucasin (5 μM; 48 h) decreases total RelA and phosphorylated RelA immunofluorescence in U87MG and LN229 cells^[1].
Napabucasin (48 h) increases apoptosis in PC-3 and 22RV1 prostate cancer cells^[3].
Napabucasin inhibits STAT3 phosphorylation and Bcl-2 expression in A549 and H1975 cells^[4].

Anti-cancer

Apoptosis

Cell Cycle Regulation

Napabucasin (5 μM; 48 h) downregulates CDK4/cyclin D1 and upregulates cleaved caspase-3/cleaved PARP in U87MG and LN229 cells^[1].
Napabucasin (5 μM; 48 h) reduces total RelA and phosphorylated RelA protein levels in U87MG and LN229 cells^[1].
Napabucasin (0.2 μM; 48 h) induces apoptosis in A549 and H1975 cells and increases G2/M phase arrest, especially in H1975 cells^[4].

Anti-cancer

Cell Cycle Regulation

Napabucasin (5 μM; 48 h) induces G0/G1 phase arrest in U87MG and LN229 cells^[1].
Napabucasin induces G1 phase accumulation and reduces S phase in PC-3 and 22RV1 prostate cancer cells^[3].

Anti-cancer

Cytokines & Chemokines

Oxidative Stress

Napabucasin (0.5-2.0 µM; 2 h) reduces STAT3 and JAK phosphorylation in pancreatic cancer cells in an NQO1- and ROS-dependent manner^[2].

Anti-cancer

Oxidative Stress

Napabucasin (0.01-5 µM; 6-24 h) reduces the viability of MiaPaCa2, AsPc1, Suit2, and Panc1 pancreatic cancer cells and induces ROS, and Dicoumarol (HY-N0645) reverses these effects in NQO1-expressing MiaPaCa2/AsPc1 and organoid-derived cells^[2].
Napabucasin (5 µM; 6 h) induces ROS and cytotoxicity in NQO1-deficient Panc1 cells; POR knockdown attenuates this effect, whereas TXNRD1 knockdown sensitizes the cells^[2].

Anti-cancer

Oxidative Stress

Cytokines & Chemokines

Napabucasin (0.5 µM; 2 h) induces NQO1-dependent oxidative stress and DNA damage transcriptome responses in MiaPaCa2 cells, including HMOX1 upregulation^[2].

Oxidative Stress

Napabucasin (1-2 µM) induces dose-dependent ROS production in DIPG-KAPP and DIPG36 cells^[7].
Napabucasin (1 µM; 24 h) combined with 4 Gy RT enhances ROS production in DIPG36 and DIPG-KAPP cells^[7].
NQO1 depletion abolishes Napabucasin (1 µM; 24 h)-mediated ROS production in DIPG36 cells^[7].
Napabucasin (24-48 h) activates ROS-related transcriptional programs in DIPG6 cells^[7].
Napabucasin (1 µM; 6 h) induces SRXN1, HMOX1, and GCLM expression in DIPG36 cells in an NQO1-dependent manner^[7].

Others

Napabucasin is a high-affinity NQO1 substrate in purified human NQO1 assays, with a K_M of 0.5 µM^[2].
Napabucasin is a POR substrate with a K_M of 2.6 µM^[2].
Napabucasin (4 μM) upregulates CCL21 mRNA, protein, and secretion in primary mouse hepatocytes and AML12 mouse hepatocytes, and upregulates CCL21 expression in MIHA human hepatocytes^[5].
Napabucasin (4 μM) induces c-Fos in primary hepatocytes and AML12 mouse hepatocytes; c-Fos knockdown inhibits CCL21 mRNA and protein secretion in AML12 cells^[5].

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

Cell Viability Assay^[1]

Cell Line:

human GBM cell lines U87MG and LN229
Concentration:

1, 5, 10 μM
Incubation Time:

24, 48, 72 h
Result:

Impaired U87MG and LN229 proliferation in a time- and dose-dependent manner.
IC50 values were 6.4 μM in U87MG cells and 5.6 μM in LN229 cells.

Cell Proliferation Assay^[1]

Cell Line:

human GBM cell lines U87MG and LN229
Concentration:

5 μM
Incubation Time:

48 h
Result:

Decreased the fraction of EdU-positive U87MG cells to 12.3% and LN229 cells to 11.7%.

Cell Proliferation Assay^[1]

Cell Line:

human GBM cell lines U87MG and LN229
Concentration:

5 μM
Incubation Time:

10 d
Result:

After Napabucasin exposure, colony-forming U87MG cells were 19.0% and LN229 cells were 14.7%.

Cell Invasion Assay^[1]

Cell Line:

human GBM cell lines U87MG and LN229
Concentration:

1 μM
Incubation Time:

24 h
Result:

Reduced the percentage of invaded U87MG cells to 26.5% and LN229 cells to 21.5%.
Western blotting showed that MMP2 and MMP9 expression was decreased after Napabucasin exposure.

Cell Invasion Assay^[1]

Cell Line:

human GBM cell lines U87MG and LN229
Concentration:

1 μM
Incubation Time:

48 h
Result:

Napabucasin-exposed spheroids showed impaired invasive behavior consistent with previous invasion results.

Cell Cycle Analysis^[1]

Cell Line:

human GBM cell lines U87MG and LN229
Concentration:

5 μM
Incubation Time:

48 h
Result:

Increased G0/G1 phase in U87MG cells to 76.7% and reduced S phase to 11.9%; in LN229 cells, G0/G1 increased to 72.3% and S phase decreased to 15.0%.

Apoptosis Analysis^[1]

Cell Line:

human GBM cell lines U87MG and LN229
Concentration:

5 μM
Incubation Time:

48 h
Result:

Increased the apoptotic ratio in U87MG cells to 35.9% and in LN229 cells to 34.2%.

Western Blot Analysis^[1]

Cell Line:

human GBM cell lines U87MG and LN229
Concentration:

5 μM
Incubation Time:

48 h
Result:

Reduced CDK4 and cyclin D1 protein levels and enhanced cleaved caspase-3 and cleaved PARP levels.\nRelative total RelA levels were 0.47 in U87MG cells and 0.43 in LN229 cells; relative phospho-RelA levels were 0.15 in U87MG cells and 0.20 in LN229 cells.

Immunofluorescence^[1]

Cell Line:

human GBM cell lines U87MG and LN229
Concentration:

5 μM
Incubation Time:

48 h
Result:

Cleaved caspase-3 was widely distributed in Napabucasin-exposed U87MG and LN229 cells.\nReduced STAT3 immunofluorescence in both U87MG and LN229 cells.\nDecreased total and phospho-RelA fluorescence intensities in U87MG and LN229 cells; RelA colocalized with STAT3 in both phosphorylated and non-phosphorylated states.

Western Blot Analysis^[1]

Cell Line:

human GBM cell lines U87MG and LN229
Concentration:

1, 5, 10 μM
Incubation Time:

48 h
Result:

Relative STAT3 protein levels in U87MG cells were 0.60, 0.20, and 0.13 at 1, 5, and 10 μM, respectively.
In LN229 cells, relative STAT3 levels were 1.08, 0.14, and 0.01 at 1, 5, and 10 μM, respectively.

Real Time qPCR^[1]

Cell Line:

U87MG-GSCs and LN229-GSCs
Concentration:

5 μM
Incubation Time:

10 d
Result:

Decreased mRNA levels in U87MG-GSCs and LN229-GSCs, respectively: STAT3 to 11.7% and 17.4%; β-catenin to 21.4% and 21.5%; c-Myc to 19.4% and 18.6%; SOX2 to 41.2% and 40.5%; OCT4 to 19.8% and 25.0%; Nestin to 35.0% and 33.9%.

Western Blot Analysis^[1]

Cell Line:

U87MG-GSCs and LN229-GSCs
Concentration:

5 μM
Incubation Time:

10 d
Result:

Decreased protein expression of STAT3, β-catenin, and c-Myc in both U87MG-GSCs and LN229-GSCs.

Cell Proliferation Assay^[3]

Cell Line:

PC-3 and 22RV1 cells
Concentration:

1 μM
Incubation Time:

48, 72, 96, and 120 h
Result:

Inhibited proliferation of PC-3 and 22RV1 cells at 48, 72, 96, and 120 h compared with control.

Cell Cytotoxicity Assay^[3]

Cell Line:

PC-3 cells
Concentration:

1 μM
Incubation Time:

48 h
Result:

Docetaxel IC₅₀ was 22.269 nM in DMSO control and 9.516 nM in PC-3 cells exposed to napabucasin.

Western Blot Analysis^[3]

Cell Line:

PrCSCs isolated from PC-3 cells
Concentration:

0, 1, 2 μM
Incubation Time:

24 h
Result:

Decreased protein expression of β-catenin, KLF-4, NANOG, Survivin, and C-myc in PrCSCs isolated from PC-3 cells in a dose-dependent manner.

Cell Proliferation Assay^[4]

Cell Line:

NSCLC cells
Concentration:

0.2 μM or 0.4 μM
Incubation Time:

2 weeks
Result:

BBI608 significantly inhibited colony formation of NSCLC cells compared with the control group.

Cell Migration Assay ^[4]

Cell Line:

A549 and H1975 cells
Concentration:

0.2 μM
Incubation Time:

24 h
Result:

BBI608 reduced the migration rate of A549 cells and H1975 cells by 8% and 13%, respectively, compared to the control group.

Apoptosis Analysis^[4]

Cell Line:

A549 and H1975 cells
Concentration:

0.2 μM
Incubation Time:

48 h
Result:

Significantly induced apoptosis in both A549 and H1975 cells.
Resulted in an increase in the number of cells in the G2/M phase, markedly in H1975 cells, indicating cell cycle arrest.

Western Blot Analysis^[4]

Cell Line:

A549/DDP cells
Concentration:

0.2 μM
Incubation Time:

48 h
Result:

The results demonstrated that BBI608 significantly inhibited the expression of p-STAT3, β-catenin and SOX-2 in A549/DDP cells.

Real Time qPCR^[7]

Cell Line:

DIPG36 WT and NQO1-depleted cells
Concentration:

1 µM
Incubation Time:

6 h
Result:

Increased SRXN1, HMOX1, and GCLM expression by 3.4-, 23.7-, and 4.0-fold, respectively.
NQO1 depletion abrogated this transcriptional effect.

In Vivo

Adaptive ImmunityCytokines & ChemokinesAnti-cancerImmune Tolerance & ImmunosuppressionApoptosisOxidative Stress

Adaptive Immunity

Cytokines & Chemokines

Napabucasin (20 mg/kg; oral; daily; 7 days) reprograms the immune microenvironment of healthy livers in C57BL/6J mice, increasing lymphocyte infiltration, effector markers, and hepatocellular CCL21 expression^[5].

Anti-cancer

Napabucasin (40 mg/kg; intraperitoneal injection; every other day; starting 7 days after tumor cell implantation) inhibits intracranial U87MG glioma growth and prolongs the survival of nude mice^[1].
Napabucasin (40 mg/kg; intraperitoneal injection; once every 3 days) inhibits the growth of PC-3 prostate cancer xenograft tumors in nude mice and tumor-derived sphere formation^[3].
Napabucasin (40 mg/kg; intraperitoneal injection; once every 3 days) inhibits the growth of 22RV1 prostate cancer xenograft tumors in nude mice and tumor-derived sphere formation^[3].
Napabucasin (20 mg/kg; oral; daily; administered 7 days before tumor inoculation) inhibits liver metastatic colonization and prolongs survival in C57BL/6J mice in the MC38 splenic liver metastasis model^[5].
Napabucasin (20 mg/kg; oral; daily; administered 7 days before tumor inoculation) does not inhibit MC38 lung metastasis in C57BL/6J mice and does not affect subcutaneous MC38 tumor growth or lymphocyte infiltration in C57BL/6J mice^[5].
Napabucasin (20 mg/kg; oral; daily; administered 7 days before tumor inoculation or continuously) reduces liver metastasis in the poorly immunogenic CT26/BALB/c model under both the pre-exposure discontinuation and continuous administration regimens^[5].
Napabucasin (20 mg/kg; oral; for 28 consecutive days) reduces the CD34⁺CD38^- leukemia cell population and prevents long-term leukemia engraftment in secondary recipients^[6].
Napabucasin (10 mg/kg; intraperitoneal injection; daily; for 5 consecutive days) in combination with radiotherapy improves local tumor control in DIPG36 and DIPG-KAPP subcutaneous xenograft models^[7].

Anti-cancer

Adaptive Immunity

Immune Tolerance & Immunosuppression

Napabucasin (20 mg/kg; oral; daily; administered 7 days before tumor inoculation) sensitizes liver MC38 tumors in C57BL/6J mice to PD-1/PD-L1 blockade and increases CD8⁺ T cell infiltration^[5].

Anti-cancer

Apoptosis

Napabucasin (20 mg/kg; oral; for 14 consecutive days) modulates Stat3/Nanog pathway biomarkers, induces p21Cip1 and cleaved PARP, and decreases BMI-1, phospho-Stat3, c-Myc, Sox-2, and Bcl-XL in T315I-BCR-ABL1-positive leukemia xenograft tumors^[6].

Anti-cancer

Oxidative Stress

Napabucasin (200 mg/kg; oral gavage; once daily; for 24 days) induces intratumoral ROS and NRF2 target gene expression in NQO1-expressing MiaPaCa2 pancreatic cancer xenografts in nude mice, but has no such effect in NQO1-knockout xenografts^[2].

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

Animal Model:

nude (female, 6 weeks old)^[1]
Dosage:

40 mg/kg in 200 μL PBS
Administration:

i.p.; every other day; starting 7 days after tumor cell implantation
Result:

Nude mice bearing intracranial U87MG xenografts exhibited significantly slower glioma proliferation by bioluminescence imaging.
Had a prolonged survival period (42.5 days) compared with the vehicle group (30.5 days).
Immunohistochemical analyses demonstrated downregulated expression levels of STAT3, MMP2, Ki-67, cyclin D1, β-catenin, and c-Myc.

Animal Model:

Nude (Charles River Laboratory, stock number 24102242)^[2]
Dosage:

200 mg/kg
Administration:

p.o. (oral gavage); once daily; for 24 days
Result:

Rintratumoral GSH:GSSG ratio in MiaPaCa2 Rosa26 xenografts, indicating ROS generation; this reduction was not observed in tumors derived from NQO1-knockout cells.
After 24 days, qPCR analysis of snap-frozen tumor samples from MiaPaCa2 Rosa26 xenografts (n=6) and MiaPaCa2 NQO1-71 xenografts (n=6) showed increased expression of HMOX1 and other NRF2 target genes in-exposed MiaPaCa2 Rosa26 tumors but not in NQO1-71 tumors.
The ROS-induced stress response was observed in MiaPaCa2 Rosa26 xenografts but not in MiaPaCa2 NQO1-knockout xenografts.

Animal Model:

nude (immunodeficient)^[3]
Dosage:

40 mg/kg
Administration:

intraperitoneal (i.p.); once every 3 days
Result:

Significantly reduced xenograft tumor growth and tumor volume compared with PBS.
No differences were observed between the this compound and docetaxel groups in PC-3 mouse xenograft tumor volume.
Significantly reduced tumor weight compared with PBS.
In tumor-derived cells, this compound inhibited spherogenesis, with numbers of spheres significantly decreased compared with PBS; docetaxel had no obvious effect on spherogenesis.

Animal Model:

nude (immunodeficient)^[3]
Dosage:

40 mg/kg
Administration:

intraperitoneal (i.p.); once every 3 days
Result:

Significantly reduced xenograft tumor growth and tumor volume compared with PBS.
In 22RV1 mouse xenografts, tumor volume in the this compound group was lower than in the docetaxel group.
Significantly reduced tumor weight compared with PBS.
In tumor-derived cells, this compound inhibited spherogenesis, with numbers of spheres significantly decreased compared with PBS; docetaxel had no obvious effect on spherogenesis.

Animal Model:

C57BL/6J (male, 6-week-old)^[5]
Dosage:

20 mg/kg
Administration:

p.o.; daily; 7 days before tumor inoculation; discontinued thereafter
Result:

Showed reduced liver metastasis, with lower liver gross weight, fewer metastatic nodules, and lower liver tumor net weight compared with controls.
No effect was observed on the primary tumor at the spleen.
H&E staining showed smaller metastatic areas in this compound-pretreated livers.
CD8+ T-cell infiltration was increased in liver metastases.
this compound-pretreated mice showed extended survival compared with controls.
In ex vivo restimulation, T cells from the MC38 liver micro-metastasis model showed increased polyfunctional CD8+ T cells; triple-positive IFN-γ+TNF-α+IL-2+ CD8+ T cells were 4.6% in control and 10.9% in this compound groups.
Did not show reduced lung metastases.
No differences in lung/body weight or metastatic area were observed between this compound-pretreated and control groups.
Had no effect on subcutaneous tumor growth.
No differences in tumor volume or tumor weight were observed between groups.
Lymphocyte infiltration (CD3+ and CD8+ cells) also showed no difference between this compound-pretreated and control groups.

Animal Model:

CT26/BALB/c (male, 6-week-old)^[5]
Dosage:

20 mg/kg
Administration:

p.o.; daily; 7 days before tumor inoculation; continuous dosing
Result:

Showed reduced liver metastasis compared with controls.
Continuous dosing also reduced metastatic burden.
The pretreated-withdrawal group still showed inhibition of liver metastasis compared with controls.

Animal Model:

C57BL/6J (male, 6-week-old)^[5]
Dosage:

20 mg/kg
Administration:

p.o.; daily; 7 days
Result:

RNA sequencing of liver tissue showed 554 upregulated genes and 176 downregulated genes after this compound exposure.
STAT3-related genes showed minimal changes; immune-related pathways were enriched.
Flow cytometry showed increased CD3+ cells (13.0% control vs 23.1% this compound), CD8+CD3+ cells (4.43% vs 16.9%), and B220+CD3− cells (24.5% vs 42.2%).
GZMB+CD8+ T cells increased from 43.3% to 70.3%, and IFN-γ+CD8+ T cells increased from 11.4% to 33.1%.
Hepatic Ccl21a and Ccr7 expression increased after this compound exposure, while Ccl21a showed no change in spleen, heart, lung, small intestine, or colon.
Immunohistochemistry localized increased CCL21 expression in hepatocytes.

Animal Model:

NOD/SCID^[6]
Dosage:

20 mg/kg
Administration:

p.o.; for 28 days
Result:

BBI608 reduced the population of CD34+CD38- cells.
Secondary recipient mice receiving human CD45+ spleen cells from this compound-exposed donors showed no detectable leukemia engraftment, whereas recipients of vehicle-exposed donor cells engrafted with leukemia.

Animal Model:

NOD/SCID^[6]
Dosage:

20 mg/kg
Administration:

p.o.; for 14 days
Result:

Induced expression of p21Cip1 and cleaved PARP.
Reduced expression of BMI-1, phospho-Stat3, c-Myc, Sox-2, and Bcl-XL.

Animal Model:

athymic nude (6-week-old)^[7]
Dosage:

10 mg/kg
Administration:

i.p.; daily; 5 consecutive days
Result:

Combination RT plus this compound improved local tumor control starting at 8 weeks post-initiation for DIPG36.

Animal Model:

B6[Cg]-Tyrc-2J/J (6-week-old)^[7]
Dosage:

10 mg/kg
Administration:

i.p.; daily; 5 consecutive days
Result:

Combination RT plus this compound improved local tumor control starting at 4 weeks post-initiation for DIPG-KAPP.

Related Protocols :

Clinical Trial

NCT Number	Sponsor	Condition	Start Date	Phase A549
NCT01329991			2011-05	PHASE1

Chemical Information

CAS. Nr. 83280-65-3
Appearance Solid
Molecular Weight 240.21
Formel C₁₄H₈O₄
Color Light yellow to green yellow
SMILES

O=C(C1=C2OC(C(C)=O)=C1)C3=C(C2=O)C=CC=C3
Synonyms

BBI608; BB608
Versand

Room temperature in continental US; may vary elsewhere.

Speicherung

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	2 years
	-20°C	1 year

Publications (29)

All WBIFFlow CytometryCell Migration/Invasion Assay2D/3D Cell Culture and DifferentiationIHCCell Proliferation/Viability Assay

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Journal Impact Factor

Cell

Cancer SLC6A6-mediated taurine uptake transactivates immune checkpoint genes and induces exhaustion in CD8+ T cells. [Abstract]

2024 Apr 25;187(9):2288-2304.e27. PMID: 38565142
J Clin Invest

IL20RB mediates tumoral response to osteoclastic niches and promotes bone metastasis of lung cancer. [Abstract]

2022 Oct 17;132(20):e157917. PMID: 36006737
J Exp Clin Cancer Res

Napabucasin, a novel STAT3 inhibitor suppresses proliferation, invasion and stemness of glioblastoma cells. [Abstract]

2019 Jul 5;38(1):289. PMID: 31277685

Napabucasin purchased from MedChemExpress. Usage Cited in: J Exp Clin Cancer Res. 2019 Jul 5;38(1):289. [Abstract]

Proliferation of glioma cells treated with Napabucasin (0-10 μM, 24-48 h) and detected by CCK-8 assays. Half maximal inhibitory concentrations (IC₅₀) of Napabucasin in U87MG and LN229 cells were 6.4 and 5.6 μM respectively.

Napabucasin purchased from MedChemExpress. Usage Cited in: J Exp Clin Cancer Res. 2019 Jul 5;38(1):289. [Abstract]

After treatment with the indicated doses of Napabucasin (0, 1, 5, and 10 μM) for 48 h, protein levels of STAT3 in U87MG and LN229 cells were evaluated by western blotting.

Napabucasin purchased from MedChemExpress. Usage Cited in: J Exp Clin Cancer Res. 2019 Jul 5;38(1):289. [Abstract]

IF was used to estimate the expression of STAT3 in U87MG and LN229 cells after treatment with Napabucasin (5 μM, 48 h) (scale bar: 50 μm).

Napabucasin purchased from MedChemExpress. Usage Cited in: J Exp Clin Cancer Res. 2019 Jul 5;38(1):289. [Abstract]

EdU incorporation assays showed that exposure to 5 μM Napabucasin for 48 h impaired DNA synthesis in U87MG and LN229 cells.

Napabucasin purchased from MedChemExpress. Usage Cited in: J Exp Clin Cancer Res. 2019 Jul 5;38(1):289. [Abstract]

Napabucasin (5 μM, 48 h) arrests the GBM cell cycle and induces apoptosis. Cell cycle distribution of glioma cells analyzed by flow cytometry.

Napabucasin purchased from MedChemExpress. Usage Cited in: J Exp Clin Cancer Res. 2019 Jul 5;38(1):289. [Abstract]

Napabucasin represses the migration and invasion of GBM cells. Representative images of the wound healing assay showing that Napabucasin treatment (1 μM, 24 h) inhibited glioma cell migration.

Napabucasin purchased from MedChemExpress. Usage Cited in: J Exp Clin Cancer Res. 2019 Jul 5;38(1):289. [Abstract]

Napabucasin impairs the stemness of GBM cells. GSCs from U87MG and LN229 cells were grown in serum-free DMEM/F12 medium with or without Napabucasin (5 μM) for 10 days. Sphere morphology was photographed under a light microscope and spheroids were counted.

Napabucasin purchased from MedChemExpress. Usage Cited in: J Exp Clin Cancer Res. 2019 Jul 5;38(1):289. [Abstract]

Napabucasin (40 mg/kg, intraperitoneal injection, every other day ) suppresses tumor growth in an orthotopic glioma model. Immunohistochemistry was used to assess the expression of STAT3, MMP2, Ki-67, cyclin D1, β-catenin, and c-Myc in orthotopic xenografted tumors after vehicle or Napabucasin treatments.
Cell Death Dis

Targeting EZH2-driven cholesterol metabolic vulnerability through Napabucasin suppresses ovarian cancer metastasis. [Abstract]

2026 Jun 27;17(1):603. PMID: 42373608
Cell Death Dis

Both direct and indirect suppression of MCL1 synergizes with BCLXL inhibition in preclinical models of gastric cancer. [Abstract]

2025 Mar 12;16(1):170. PMID: 40075071
Phytomedicine

β, β-Dimethylacrylshikonin potentiates paclitaxel activity, suppresses immune evasion and triple negative breast cancer progression via STAT3Y705 phosphorylation inhibition based on network pharmacology and transcriptomics analysis. [Abstract]

2023 Jun:114:154769. PMID: 36940580
Oncogene

RAF1 contributes to cell proliferation and STAT3 activation in colorectal cancer independently of microsatellite and KRAS status. [Abstract]

2023 May;42(20):1649-1660. PMID: 37020037
Clin Transl Med

Inhibition of ROCK ameliorates pulmonary fibrosis by suppressing M2 macrophage polarisation through phosphorylation of STAT3. [Abstract]

2022 Oct;12(10):e1036. PMID: 36178087
Cell Rep

AKTIP loss is enriched in ERα-positive breast cancer for tumorigenesis and confers endocrine resistance. [Abstract]

2022 Dec 13;41(11):111821. PMID: 36516775
J Med Chem

A Novel Redox Modulator Induces a GPX4-Mediated Cell Death That Is Dependent on Iron and Reactive Oxygen Species. [Abstract]

2020 Sep 10;63(17):9838-9855. PMID: 32809827
Sci Signal

The E3 ligase TRIM21 promotes progression of pancreatic ductal adenocarcinoma by down-regulating TAp63α and derepressing IL20RB. [Abstract]

2025 Jun 3;18(889):eadv4579. PMID: 40460193
Cells

STAT3 Inhibitor ODZ10117 Suppresses Glioblastoma Malignancy and Prolongs Survival in a Glioblastoma Xenograft Model. [Abstract]

2020 Mar 15;9(3):722. PMID: 32183406
Cancer Biol Ther

Inhibition of STAT3-mediated glycolysis by bruceine D suppresses non-small-cell lung cancer progression in vitro and in vivo. [Abstract]

2026 Dec 31;27(1):2665867. PMID: 42100892
Int Immunopharmacol

Acetylshikonin alleviates pulmonary fibrosis through inhibition of the STAT3 signaling pathway. [Abstract]

2026 Jan 1;168(Pt 1):115811. PMID: 41232362
Oncol Rep

In vitro assessment of BBI608 in 2D and 3D culture models for drug repositioning in oral squamous cell carcinoma. [Abstract]

2025 Aug;54(2):97. PMID: 40539433
J Biol Chem

STAT3 activation of SCAP-SREBP-1 signaling upregulates fatty acid synthesis to promote tumor growth. [Abstract]

2024 Jun;300(6):107351. PMID: 38718868
J Nat Prod

Telocinobufagin Has Antitumor Effects in Non-Small-Cell Lung Cancer by Inhibiting STAT3 Signaling. [Abstract]

2022 Apr 22;85(4):765-775. PMID: 35200033
Cancer Med

Suppression of prostate cancer progression by cancer cell stemness inhibitor napabucasin. [Abstract]

2016 Jun;5(6):1251-8. PMID: 26899963

Napabucasin purchased from MedChemExpress. Usage Cited in: Cancer Med. 2016 Jun;5(6):1251-8. [Abstract]

Representative images of colony formation assay in PCa cell lines (PC-3 and 22RV1) and histological analysis of the colony number show that the colony formation of PCa cell lines are dramatically decreased after treated with 1 μM Napabucasin for 24 h.
J Cancer

Cinobufagin exerts an antitumor effect in non-small-cell lung cancer by blocking STAT3 signaling. [Abstract]

2023 Oct 2;14(17):3309-3320. PMID: 37928418
J Clin Med

Development of Oxadiazole-Based ODZ10117 as a Small-Molecule Inhibitor of STAT3 for Targeted Cancer Therapy. [Abstract]

2019 Nov 2;8(11):1847. PMID: 31684051
Med Sci Monit

Napabucasin Attenuates Resistance of Breast Cancer Cells to Tamoxifen by Reducing Stem Cell-Like Properties. [Abstract]

2019 Nov 24:25:8905-8912. PMID: 31760402
Onco Targets Ther

Bone Marrow-Derived Myofibroblasts Promote Gastric Cancer Metastasis by Activating TGF-β1 and IL-6/STAT3 Signalling Loop. [Abstract]

2020 Oct 16:13:10567-10580. PMID: 33116635
Arch Oral Biol

BBI608 induces apoptosis in mucoepidermoid carcinoma cells by targeting a post-transcriptional regulatory mechanisms of myeloid cell leukemia-1. [Abstract]

2026 Feb:182:106467. PMID: 41352329
Acta Cir Bras

Effect of napabucasin and doxorubicin via the Jak2/Stat3 signaling pathway in suppressing the proliferation of neuroblastoma cells. [Abstract]

2024 Sep 30:39:e396624. PMID: 39356934
Res Sq

2026 Jul 3.
bioRxiv

2026 Mar 26.
Universidad de Las Palmas de Gran Canaria

2023 May 24.
University of Michigan

2020 Oct.
Methods Mol Biol

Homocysteine, Thioretinaco Ozonide, and Oxidative Phosphorylation in Cancer and Aging: A Proposed Clinical Trial Protocol. [Abstract]

2019:1866:285-310. PMID: 30725425

Lösungsmittel & Löslichkeit

In Vitro:

N-Methylpyrrolidone (NMP) : 16.67 mg/mL (69.40 mM; Need ultrasonic)

DMSO : 4.44 mg/mL (18.48 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

H₂O : < 0.1 mg/mL (insoluble)

Ethanol : < 1 mg/mL (insoluble)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

4.1630 mL

20.8151 mL

41.6302 mL

5 mM

0.8326 mL

4.1630 mL

8.3260 mL

10 mM

0.4163 mL

2.0815 mL

4.1630 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 5% NMP 40% PEG300 5% Tween-80 50% Saline

Solubility: 0.83 mg/mL (3.46 mM); Suspended solution; Need ultrasonic

Protocol 2

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: 0.5 mg/mL (2.08 mM); Suspended solution; Need ultrasonic

This protocol yields a suspended solution of 0.5 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (5.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 3

Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)

Solubility: 0.5 mg/mL (2.08 mM); Suspended solution; Need ultrasonic

This protocol yields a suspended solution of 0.5 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (5.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

Protocol 4

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 0.5 mg/mL (2.08 mM); Clear solution

This protocol yields a clear solution of ≥ 0.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (5.0 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
Saline +

The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (334 KB)
SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
- Norwegian - NO (394 KB)
- Español - ES (394 KB)
- Swedish - SV (394 KB)
- Italian - IT (394 KB)
- Korean - KR (394 KB)
- Portuguese - PT (394 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)
Handling Instructions (2659 KB)

Verweise

[1]. Han D, et al. Napabucasin, a novel STAT3 inhibitor suppresses proliferation, invasion and stemness of glioblastoma cells. Journal of experimental & clinical cancer research : CR. 2019 Jul 05;38(1):289. [Content Brief]

[2]. Froeling FEM, et al. Bioactivation of Napabucasin Triggers Reactive Oxygen Species-Mediated Cancer Cell Death. Clinical cancer research : an official journal of the American Association for Cancer Research. 2019 Dec 01;25(23):7162-7174.

[3]. Zhang Y, et al. Suppression of prostate cancer progression by cancer cell stemness inhibitor napabucasin. Cancer medicine. 2016 Jun;5(6):1251-8. [Content Brief]

[4]. Feng Q, et al. A redox-responsive nanosystem to suppress chemoresistant lung cancer through targeting STAT3. Journal of controlled release : official journal of the Controlled Release Society. 2023 Nov;363:349-360.

[5]. Wang Q, et al. Napabucasin transforms liver microenvironment and boosts immunotherapy efficacy by converting potential metastases into “hot” tumors. Interdisciplinary Medicine. 2026 May;4(3):e70089.

[6]. Tauchi T, et al. Activity of the Stemness Inhibitor, BBI608, on the Self-Renewal of BCR-ABL1 Positive Leukemia Cells: Molecular Mechanisms. Blood. 2014 Dec 6;124(21):905.

[7]. Gallitto M, et al. Targeted delivery of napabucasin with radiotherapy improves outcomes in diffuse midline glioma. Neuro-oncology. 2025 Mar 07;27(3):795-810.

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.

Complete Stock Solution Preparation Table

Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO / N-Methylpyrrolidone (NMP)	1 mM	4.1630 mL	20.8151 mL	41.6302 mL	104.0756 mL
	5 mM	0.8326 mL	4.1630 mL	8.3260 mL	20.8151 mL
	10 mM	0.4163 mL	2.0815 mL	4.1630 mL	10.4076 mL
	15 mM	0.2775 mL	1.3877 mL	2.7753 mL	6.9384 mL
N-Methylpyrrolidone (NMP)	20 mM	0.2082 mL	1.0408 mL	2.0815 mL	5.2038 mL
	25 mM	0.1665 mL	0.8326 mL	1.6652 mL	4.1630 mL
	30 mM	0.1388 mL	0.6938 mL	1.3877 mL	3.4692 mL
	40 mM	0.1041 mL	0.5204 mL	1.0408 mL	2.6019 mL
	50 mM	0.0833 mL	0.4163 mL	0.8326 mL	2.0815 mL
	60 mM	0.0694 mL	0.3469 mL	0.6938 mL	1.7346 mL

Bioz

Napabucasin

29 Cited Publications

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Napabucasin

Publications Citing Use of MedChemExpress (MCE) Napabucasin

Alle STAT Isoform-spezifische Produkte anzeigen

Alle NF-κB Isoform-spezifische Produkte anzeigen

Biologische Aktivität

Beschreibung

IC₅₀ & Target

Cellular Effect

In Vitro

In Vivo

Clinical Trial

Chemical Information

Publications (29)

Lösungsmittel & Löslichkeit

In Vitro:

In Vivo:

In Vivo Dissolution Calculator

Reinheit & Dokumentation

Verweise

Help & FAQs

Complete Stock Solution Preparation Table

Bioz

Keywords

Your Recently Viewed Products

Napabucasin

Publications Citing Use of MedChemExpress (MCE) Napabucasin

Alle STAT Isoform-spezifische Produkte anzeigen

Alle NF-κB Isoform-spezifische Produkte anzeigen

Biologische Aktivität

Beschreibung

IC50 & Target

Cellular Effect

In Vitro

In Vivo

Clinical Trial

Chemical Information

Publications (29)

Lösungsmittel & Löslichkeit

In Vitro:

In Vivo:

In Vivo Dissolution Calculator

Reinheit & Dokumentation

Verweise

Help & FAQs

Complete Stock Solution Preparation Table

Napabucasin Related Classifications

HY-13919 Related Classifications

Bioz

Keywords

Your Recently Viewed Products

IC₅₀ & Target