OSU-53
OSU-53 is an orally active AMPK activator and mTOR inhibitor, with an IC50 of 0.3 μM for AMPK, an EC50 of 2-5 μM for AMPK, and an IC50 of 8.23 μM for mTOR. OSU-53 inhibits the Akt signaling pathway, directly activates AMPK by binding to its autoinhibitory domain, reduces IKKβ-mediated phosphorylation of Foxo3a, blocks Akt-mediated phosphorylation of MDM2, and promotes the nuclear localization and stabilization of Foxo3a, while directly inhibiting mTOR. OSU-53 inhibits epithelial-mesenchymal transition (EMT), induces epithelial phenotype, suppresses invasion and metastasis, induces autophagy, inhibits the activation of ERK and Akt, reduces the secretion of nitric oxide and proinflammatory cytokines, and inhibits the migration of MDSC; at high doses, it induces MDSC apoptosis, attenuates the immunosuppressive effect of MDSC, reduces MDSC levels, and blocks incision-induced mechanical hyperalgesia. OSU-53 can be used in studies related to breast cancer, prostate cancer, thyroid cancer, melanoma and postoperative pain.
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- CAS 番号: 1290069-19-0
- 分子式: C25H24F3N3O6S2
- 分子量:583.60
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
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製品説明
OSU-53 is an orally active AMPK activator and mTOR inhibitor, with an IC50 of 0.3 μM for AMPK, an EC50 of 2-5 μM for AMPK, and an IC50 of 8.23 μM for mTOR. OSU-53 inhibits the Akt signaling pathway, directly activates AMPK by binding to its autoinhibitory domain, reduces IKKβ-mediated phosphorylation of Foxo3a, blocks Akt-mediated phosphorylation of MDM2, and promotes the nuclear localization and stabilization of Foxo3a, while directly inhibiting mTOR. OSU-53 inhibits epithelial-mesenchymal transition (EMT), induces epithelial phenotype, suppresses invasion and metastasis, induces autophagy, inhibits the activation of ERK and Akt, reduces the secretion of nitric oxide and proinflammatory cytokines, and inhibits the migration of MDSC; at high doses, it induces MDSC apoptosis, attenuates the immunosuppressive effect of MDSC, reduces MDSC levels, and blocks incision-induced mechanical hyperalgesia. OSU-53 can be used in studies related to breast cancer, prostate cancer, thyroid cancer, melanoma and postoperative pain[1][2][3][4].
|
AMPK 0.3 μM (IC50) |
AMPK 2-5 μM (EC50) |
mTOR 8.23 μM (IC50) |
Akt |
IKKβ |
FOXO3a |
MDM2 |
MDSC |
Cellular Effect
|
Cell Line
|
Type | Value | Description | References |
|---|---|---|---|---|
| MCF7 | IC50 |
5 μM
|
Antiproliferative activity against human MCF-7 cancer cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
Antiproliferative activity against human MCF-7 cancer cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
|
24994714 |
| MDA-MB-231 | IC50 |
7.5 μM
|
Antiproliferative activity against human MDA-MB-231 cancer cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
Antiproliferative activity against human MDA-MB-231 cancer cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
|
24994714 |
| MDA-MB-468 | IC50 |
5 μM
|
Antiproliferative activity against human MDA-MB-468 cancer cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
Antiproliferative activity against human MDA-MB-468 cancer cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
|
24994714 |
| 4T1 | IC50 |
6 μM
|
Antiproliferative activity against mouse 4T1 cancer cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
Antiproliferative activity against mouse 4T1 cancer cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
|
24994714 |
| LNCaP | IC50 |
9 μM
|
Antiproliferative activity against human LNCaP cancer cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
Antiproliferative activity against human LNCaP cancer cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
|
24994714 |
| DU-145 | IC50 |
8 μM
|
Antiproliferative activity against human DU-145 cancer cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
Antiproliferative activity against human DU-145 cancer cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
|
24994714 |
| PC-3 | IC50 |
5 μM
|
Antiproliferative activity against human PC-3 cancer cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
Antiproliferative activity against human PC-3 cancer cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
|
24994714 |
体外実験
Anti-cancerApoptosisInnate ImmunityImmune Tolerance & ImmunosuppressionCytokines & ChemokinesAutophagyOthers
Anti-cancer
OSU-53 (5-10 μM; 72 h) inhibits the viability of MCF-7, MDA-MB-231, MDA-MB-468, 4T1, LNCaP, DU-145, and PC-3 cancer cell lines with IC50 values of 5 μM, 7.5 μM, 5 μM, 6 μM, 9 μM, 8 μM, and 5 μM respectively after 72 h of treatment, and has no antiproliferative effect on normal MECs and PrECs[1].
OSU-53 (2.5-10 μM) reverses the mesenchymal phenotype of MDA-MB-231, 4T1, PC-3, and MDA-MB-468 cells via AMPK activation, inducing increased expression of epithelial markers and decreased expression of mesenchymal markers at the mRNA and/or protein level[1].
OSU-53 (5 μM) induces Foxo3a binding to the FBE3 and FBE4 regions of the E-cadherin promoter in MDA-MB-468, PC-3, and MDA-MB-231 cells[1].
OSU-53 (5 μM; 24 h) promotes nuclear localization of Foxo3a and cytoplasmic sequestration of MDM2 in MDA-MB-231, 4T1, and PC-3 cells by suppressing Akt and IKKβ phosphorylation[1].
OSU-53 (5 μM; 12 h) increases Foxo3a protein stability by reducing MDM2-mediated ubiquitination in cancer cells, an effect blocked by ectopic MDM2 or constitutively active Akt expression[1].
OSU-53 (1-10 μM; 24-72 h) inhibits the proliferation of all tested human thyroid cancer cell lines in a dose-dependent manner, with greatest potency (GI50 1.63-4.51 μM) in lines with activating RAS or BRAFV600E mutations, and lower potency (GI50 5.90-7.26 μM) in FTC133 and TPC1 cells[3].
OSU-53 (5 μM; 6-72 h) activates AMPK, suppresses mTOR signaling, and modulates ERK and AKT activation in human ATC cell lines, with cell-specific differences based on RAS or BRAFV600E mutation status[3].
OSU-53 (1-10 μM; 6-72 h) activates AMPK in BCPAP and FTC133 human DTC cell lines, suppresses mTOR signaling in all three tested DTC lines, and modulates ERK and AKT activation in a cell-specific manner[3].
OSU-53 (1-10 μM; 24-72 h; 5 μM; 24-48 h) does not rely primarily on AMPK activation for induced growth inhibition or autophagy in BCPAP and FTC133 human DTC cell lines, though AMPK contributes partially to mTOR/p70S6K signaling suppression in these cells[3].
OSU-53 (0.01-15 μM; cell-free assay; 1-10 μM; 24 h) directly inhibits mTOR activity in a cell-free system (IC50 8.23 μM) and reduces mTOR phosphorylation in U-Hth-7 and Hth-104 human thyroid cancer cell lines[3].
OSU-53 (2.5-10 μM) reverses the mesenchymal phenotype of MDA-MB-231, 4T1, PC-3, and MDA-MB-468 cells via AMPK activation, inducing increased expression of epithelial markers and decreased expression of mesenchymal markers at the mRNA and/or protein level[1].
OSU-53 (5 μM) induces Foxo3a binding to the FBE3 and FBE4 regions of the E-cadherin promoter in MDA-MB-468, PC-3, and MDA-MB-231 cells[1].
OSU-53 (5 μM; 24 h) promotes nuclear localization of Foxo3a and cytoplasmic sequestration of MDM2 in MDA-MB-231, 4T1, and PC-3 cells by suppressing Akt and IKKβ phosphorylation[1].
OSU-53 (5 μM; 12 h) increases Foxo3a protein stability by reducing MDM2-mediated ubiquitination in cancer cells, an effect blocked by ectopic MDM2 or constitutively active Akt expression[1].
OSU-53 (1-10 μM; 24-72 h) inhibits the proliferation of all tested human thyroid cancer cell lines in a dose-dependent manner, with greatest potency (GI50 1.63-4.51 μM) in lines with activating RAS or BRAFV600E mutations, and lower potency (GI50 5.90-7.26 μM) in FTC133 and TPC1 cells[3].
OSU-53 (5 μM; 6-72 h) activates AMPK, suppresses mTOR signaling, and modulates ERK and AKT activation in human ATC cell lines, with cell-specific differences based on RAS or BRAFV600E mutation status[3].
OSU-53 (1-10 μM; 6-72 h) activates AMPK in BCPAP and FTC133 human DTC cell lines, suppresses mTOR signaling in all three tested DTC lines, and modulates ERK and AKT activation in a cell-specific manner[3].
OSU-53 (1-10 μM; 24-72 h; 5 μM; 24-48 h) does not rely primarily on AMPK activation for induced growth inhibition or autophagy in BCPAP and FTC133 human DTC cell lines, though AMPK contributes partially to mTOR/p70S6K signaling suppression in these cells[3].
OSU-53 (0.01-15 μM; cell-free assay; 1-10 μM; 24 h) directly inhibits mTOR activity in a cell-free system (IC50 8.23 μM) and reduces mTOR phosphorylation in U-Hth-7 and Hth-104 human thyroid cancer cell lines[3].
Apoptosis
Innate Immunity
OSU-53 (0.5-5 μM; 12 h pre-incubation plus 24 h LPS stimulation) reduces nitric oxide production in LPS-stimulated murine MDSC cell line MSC-2, with a 3-fold decrease observed at 5 μM treatment[2].
Anti-cancer
Immune Tolerance & Immunosuppression
OSU-53 (0.5-5 μM; overnight) reduces migration of the murine MDSC cell line MSC-2 toward tumor cell-derived chemoattractants, with a significant decrease observed at 5 μM treatment[2].
Cytokines & Chemokines
Innate Immunity
Anti-cancer
Autophagy
OSU-53 (5 μM; 24-48 h) induces autophagy in human thyroid cancer cell lines with RAS or BRAFV600E mutations, but does not induce meaningful apoptosis in any of the tested lines[3].
Others
OSU-53 directly activates recombinant AMPK α1β1γ2 protein with an IC50 of 0.3 μM[1].
OSU-53 (18 h) dose-dependently inhibits the migration of MDA-MB-231 and PC-3 cells, with effects independent of cell viability reduction[1].
OSU-53 (24 h) dose-dependently inhibits the invasion of MDA-MB-231 and PC-3 cells, with effects independent of cell viability reduction[1].
OSU-53 (9-16 days) dose-dependently inhibits the formation of invasive, stellate colonies by MDA-MB-231 and PC-3 cells in three-dimensional culture[1].
OSU-53 reduces F-actin stress fiber formation in MDA-MB-231 cells[1].
OSU-53 (1-5 μM; 18 h) activates AMPK in the murine MDSC cell line MSC-2, as shown by increased p-AMPK levels following 5 μM treatment for 18 hours, without changing total AMPK levels[2].
OSU-53 (18 h) dose-dependently inhibits the migration of MDA-MB-231 and PC-3 cells, with effects independent of cell viability reduction[1].
OSU-53 (24 h) dose-dependently inhibits the invasion of MDA-MB-231 and PC-3 cells, with effects independent of cell viability reduction[1].
OSU-53 (9-16 days) dose-dependently inhibits the formation of invasive, stellate colonies by MDA-MB-231 and PC-3 cells in three-dimensional culture[1].
OSU-53 reduces F-actin stress fiber formation in MDA-MB-231 cells[1].
OSU-53 (1-5 μM; 18 h) activates AMPK in the murine MDSC cell line MSC-2, as shown by increased p-AMPK levels following 5 μM treatment for 18 hours, without changing total AMPK levels[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[1]
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Cell Line:MCF-7, MDA-MB-231, MDA-MB-468, 4T1, LNCaP, DU-145, PC-3, normal mammary epithelial cells (MECs), normal prostate epithelial cells (PrECs)
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Concentration:5-10 μM
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Incubation Time:72 h
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Result:Inhibited viability of seven cancer cell lines with IC50 values of 5 μM, 7.5 μM, 5 μM, 6 μM, 9 μM, 8 μM, and 5 μM respectively after 72 h.
Exhibited no antiproliferative effect on normal MECs and PrECs.
Apoptosis Analysis[2]
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Cell Line:murine MDSC cell line MSC-2
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Concentration:0.5 μM, 1 μM, 5 μM, 10 μM
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Incubation Time:18 h (0.5 μM, 1 μM, 5 μM); overnight (10 μM)
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Result:Did not induce apoptosis in MSC-2 cells at concentrations up to 5 μM.
Caused a significant increase in apoptotic cells at the 10 μM concentration.
Western Blot Analysis[2]
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Cell Line:murine MDSC cell line MSC-2
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Concentration:1 μM, 5 μM
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Incubation Time:18 h
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Result:Did not alter total AMPK protein levels in MSC-2 cells.
Induced an increase in phosphorylated AMPK (p-AMPK) levels at 5 μM.
Cell Migration Assay [2]
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Cell Line:murine MDSC cell line MSC-2
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Concentration:0.5 μM, 1 μM, 5 μM
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Incubation Time:overnight
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Result:Caused a significant reduction in the number of MSC-2 cells migrating toward tumor cell supernatant at 5 μM compared to controls.
ELISA Assay[2]
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Cell Line:murine MDSC cell line MSC-2
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Concentration:0.5 μM, 1 μM, 5 μM
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Incubation Time:24 h
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Result:Caused a 1.5-fold decrease in TNF-α levels at 5 μM in LPS-stimulated MSC-2 cells.
Caused a 2.9-fold decrease in IL-6 levels at 5 μM in LPS-stimulated MSC-2 cells.
Cell Proliferation Assay[3]
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Cell Line:C643, U-Hth-7, SW1736, Hth-104, FTC133, TPC1, BCPAP
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Concentration:1 μM, 5 μM, 10 μM
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Incubation Time:24 h; 48 h; 72 h
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Result:Inhibited proliferation of all 7 thyroid cancer cell lines in a dose-dependent manner.
Reduced GI50 values to 1.63-4.51 μM in cell lines with activating RAS or BRAF V600E mutations.
Resulted in a GI50 of 5.90 μM in FTC133 (PTEN null) cells.
Resulted in a GI50 of 7.26 μM in TPC1 (RET/PTC1) cells.
Caused significantly less growth inhibition in FTC133 and TPC1 compared to BCPAP at 5 μM.
Western Blot Analysis[3]
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Cell Line:C643, U-Hth-7, SW1736, Hth-104
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Concentration:5 μM
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Incubation Time:6 h; 12 h; 24 h; 48 h; 72 h
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Result:Induced time-dependent activation of AMPK (increased p-AMPK relative to total AMPK) in all four ATC cell lines.
Reached peak AMPK activation at 12 hours and declined by 48 hours in RAS mutant lines (C643, U-Hth-7).
Activated TSC2 (increased p-TSC2) in three of the four cell lines, with no appreciable increase in C643.
Suppressed mTOR signaling (decreased p-p70S6K and p-S6) across all four cell lines.
Suppressed ERK activation (decreased p-ERK) after 48 hours in BRAF V600E mutant lines (SW1736, Hth-104) but not consistently in RAS mutant lines.
Down-regulated AKT activation (decreased p-AKT) in C643, U-Hth-7, and SW1736, but not Hth-104.
Western Blot Analysis[3]
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Cell Line:BCPAP, FTC133, TPC1, Hth-104
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Concentration:5 μM; 1, 2.5, 5, 7.5, 10 μM
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Incubation Time:6 h; 12 h; 24 h; 48 h; 72 h (5 μM treatment); 24 h (Hth-104 dose-response); 48 h (FTC133, TPC1 dose-response)
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Result:Induced time-dependent AMPK activation (increased p-AMPK) in BCPAP and FTC133, but not TPC1, with 5 μM treatment.
Suppressed p-p70S6K activation in all three DTC cell lines, with complete abolition of p-p70S6K in BCPAP after 6 hours.
Induced time-dependent inactivation of ERK (decreased p-ERK) in FTC133, with variable inactivation in BCPAP and TPC1.
Induced time-dependent inactivation of AKT (decreased p-AKT) in FTC133 and TPC1, but not BCPAP.
Caused modest dose-dependent AMPK activation in Hth-104 and FTC133, but not TPC1, with dose-response treatment.
Decreased p-p70S6K in all three cell lines with dose-response treatment.
Western Blot Analysis[3]
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Cell Line:C643, U-Hth-7, SW1736, Hth-104, BCPAP, FTC133, TPC1
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Concentration:5 μM
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Incubation Time:6 h; 12 h; 24 h; 48 h; 72 h
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Result:Induced increased conversion of LC3 I to LC3 II (autophagy marker) in all BRAF V600E mutant lines (BCPAP, Hth-104, SW1736) and RAS mutant lines (C643, U-Hth-7).
Caused modest LC3 I/II conversion in TPC1 and absent conversion in FTC133.
Induced a slight increase in PARP cleavage (apoptosis marker) only in U-Hth-7 after 48 hours of treatment.
体内実験
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/cAnNCr (female, 5-7 weeks of age, syngeneic orthotopic breast cancer model via injection of 4T1 cells)[1]
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Dosage:50 mg/kg; 100 mg/kg
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Administration:p.o.; daily; 21 days
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Result:Exhibited no changes in body weight.
Modestly inhibited primary tumor growth.
Dose-dependently increased phosphorylation of AMPK and ACC, reduced phosphorylation of Akt, and increased Foxo3a expression in tumor lysates.
Increased E-cadherin levels and decreased vimentin, YB-1, Snail, and Twist levels in tumor lysates.
Reduced the number and size of metastatic nodules on the lung surface relative to controls.
Related Protocols :
- Western Blot
- Annexin V plus membrane-impermeant dye apoptosis staining
- Cell migration
- Breast Cancer Modeling
- Kinase activity and phosphorylation assays
- Detection of Apoptosis
- TUNEL staining for apoptotic DNA fragmentation
- Research Protocol for Endocrine Diseases
- Autophagy
- Apoptosis Solutions
- Cell invasion
- Protocol for Kinase activity and phosphorylation assays
- Lysosome and acidic-vesicle live-cell staining
- Macroautophagy Solutions
- Orthotopic Cell-Line Xenograft
化学情報
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CAS 番号 1290069-19-0
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分子量 583.60
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分子式 C25H24F3N3O6S2
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SMILES
O=S(C1=CC=C([N+]([O-])=O)C(C(F)(F)F)=C1)(NC2=CC=C(/C=C(SC(N3CC4(C)CCCCC4)=O)/C3=O)C=C2)=O
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
純度とドキュメンテーション
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純度:
99.98%
Assay:
99.98%
ee.:
99.98%
参考文献
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OSU-53 関連分類
HY-125535 関連分類
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