2. JAK/STAT Signaling Stem Cell/Wnt Metabolic Enzyme/Protease Apoptosis Autophagy MAPK/ERK Pathway Protein Tyrosine Kinase/RTK Epigenetics PI3K/Akt/mTOR Cell Cycle/DNA Damage
  3. STAT Phosphatase Apoptosis Autophagy p38 MAPK EGFR JAK Bcl-2 Family Survivin Akt mTOR PARP Caspase Atg8/LC3 CDK
  4. Isocryptotanshinone

Isocryptotanshinone is a dual STAT3 and PTP1B (IC50 = 56.1 μM) inhibitor. Isocryptotanshinone inhibits STAT3 by binding to the STAT3 SH2 domain to block phosphorylation and nuclear translocation[1][2]. Isocryptotanshinone exerts its anti-proliferative effect via the induction of cell cycle arrest, apoptosis, and pro-death autophagy, through the regulation of STAT3, AKT/mTOR and MAPK signaling pathways. Isocryptotanshinone suppresses the xenograft gastric cancer (GC) tumor growth in BALB/c nude mice. Isocryptotanshinone can be used for cancer research, such as lung cancer, breast cancer and GC.

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

Isocryptotanshinone

Isocryptotanshinone Chemical Structure

CAS No. : 22550-15-8

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Isocryptotanshinone Related Antibodies

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STAT3 STAT5 STAT6 STAT1

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p38 MAPK Akt1 p38α p38β MAPK13 p38δ p38γ

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CDK1 CDK2 CDK3 CDK4 CDK5 CDK6 CDK7 CDK8 CDK9 CDK11 CDK12 CDK13 CDK14 CDK16 CDK19 CDC CLK Pho85 CDK10 CDK15 CDK17 CDK18 CDK20 PITSLRE

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Description

Isocryptotanshinone is a dual STAT3 and PTP1B (IC50 = 56.1 μM) inhibitor. Isocryptotanshinone inhibits STAT3 by binding to the STAT3 SH2 domain to block phosphorylation and nuclear translocation[1][2]. Isocryptotanshinone exerts its anti-proliferative effect via the induction of cell cycle arrest, apoptosis, and pro-death autophagy, through the regulation of STAT3, AKT/mTOR and MAPK signaling pathways. Isocryptotanshinone suppresses the xenograft gastric cancer (GC) tumor growth in BALB/c nude mice. Isocryptotanshinone can be used for cancer research, such as lung cancer, breast cancer and GC[1][3][4].

IC50 & Target[1][2]

STAT3

 

PTP1B

56.1 μM (IC50)

In Vitro

Isocryptotanshinone (ICTS) (0-5 μM, 0-24 h) inhibits the constitutive STAT3 and p-STAT3 expression in A549 cells in a concentration- and time-dependent manner[1].
Isocryptotanshinone (5 μM, 12 h) decreases STAT3 in the cytoplasm and p-STAT3 in nucleus in A549 cells[1].
Isocryptotanshinone (5 μM, 0-4 h) inhibits the IL-6 (25 ng/mL)-stimulated expression of p-STAT3 in A549 cells in a time-dependent manner and almost completely abolishes p-STAT3 expression after 4 h[1].
Isocryptotanshinone (0-10 μM, 0-24 h) attenuates the expression of survival-related proteins (Bcl-2, Bcl-xL, survivin, Mcl-1) in a time-dependent manner, and suppresses the expression of upstream regulators (EGFR and JAK2) in a concentration-dependent manner[1].
Isocryptotanshinone (0-20 μM, 0-24 h) significantly inhibits the proliferation of A549 and 95D lung cancer cells in a concentration-dependent manner and induces apoptosis in A549 cells by remarkably increasing early apoptotic cell fractions, caspase 3/7 activity, and the expression of cleaved PARP[1].
Isocryptotanshinone (0-10 μM, 0-24 h) induces pro-death autophagy in A549 cells by upregulating LC3II expression, promoting the accumulation of autophagic vacuoles and autolysosomes, and inhibiting the AKT/mTOR signaling pathway, similar to Cryptotanshinone (HY-N0174)[1].
Isocryptotanshinone (0-20 μM, 24 h) inhibits proliferation (IC50 = 12.5 μM) and colony formation in MCF-7 cells by inducing G1 phase cell cycle arrest and triggering early apoptosis[3].
Isocryptotanshinone (2.5-10 μM, 0-24 h) triggers MAPK signaling activation in MCF-7 cells, which is characterized by the time- and concentration-dependent phosphorylation of JNK, ERK, and p38 MAPK[3].
Isocryptotanshinone (0-40 μM, 0-72 h) suppressed the proliferation of GC cells, with IC50 of 6.77 μM for SGC-7901 cells and 33.1 μM for MKN-45 cells[4].
Isocryptotanshinone (0-40 μM, 24 h) induces G1/G0 phase cell cycle arrest and apoptosis in GC cells (SGC-7901 and MKN-45), an effect mediated through the inhibition of the STAT3 signaling pathway and the subsequent downregulation of cell cycle- and apoptosis-associated proteins (Cyclin D1, E2F1, Mcl-1, Bcl-2, survivin)[4].

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

Isocryptotanshinone Related Antibodies

Western Blot Analysis[3]

Cell Line: MCF-7 cells
Concentration: 2.5, 5 and 10 μM
Incubation Time: 0, 1, 3, 6, 12, and 24 h
Result: Induced phosphorylation of JNK (p-JNK), ERK (p-ERK), and p38 (p-p38) in MCF-7 cells without affecting total JNK, ERK, or p38, in a time- and concentration-dependent manner.
Increased the phosphorylation of JNK, ERK, and p38 at 10 μM.

Cell Viability Assay[1][3]

Cell Line: MCF-7, MDA-MB-231, HepG2, A549, and 95D cells
Concentration: 0-40 μM
Incubation Time: 24 h
Result: Significantly inhibited the proliferation of MCF-7, MDA-MB-231, HepG2, A549 and 95D cells in a concentration-dependent manner.
Exhibited approximately 20% and 60% cell viability rates for A549 and 95D cells at 10 μM, respectively.

Western Blot Analysis[4]

Cell Line: SGC-7901 and MKN-45 cells
Concentration: 0,2.5, 5, 10, 20 and 40 μM
Incubation Time: 24 h
Result: Significantly downregulated the phosphorylation of Rb at Ser-807/811, and the expression of Cyclin D1 and E2F1 at 20 or 40 μM in SGC-7901 cells.
Decreased the expression levels of Mcl-1, Bcl-2, and Survivin at 20 and 40 μM in SGC-7901 cells.
Induced the same changes of protein marker in MKN-45 cells.
Inhibited the phosphorylation of STAT3 at Tyr-705 in a dose-dependent manner and had weak effect on the total protein.
Increased the phosphorylation of Akt at Ser-473 and no significant effects were observed on the phosphorylation of Erk1/2 at Thr-202/Tyr-204.
Decreased the expression levels of Akt and Erk1/2 at a higher concentration.
Significantly suppressed the IL-6 (25 ng/ml)-induced phosphorylation of STAT3 in SGC-7901 cells.
Inhibited the increase of the expression of Cyclin D1, p-Rb, and Survivin in SGC-7901 cells.
Suppressed the restored proliferation and the expression of Cyclin D1, p-Rb, and Survivin that were enhanced by STAT3 overexpression.

Western Blot Analysis[1]

Cell Line: A549 cells
Concentration: 0, 2, 5, 7 and 10 μM
Incubation Time: 0, 2, 6, 12, and 24 h
Result: Reduced STAT3 and p-STAT3 levels in a dose-dependent manner.
Reduced p-STAT3 levels in a time-dependent manner.
Decreased Bcl-2, Bcl-xL, Mcl-1, and survivin levels in a time-dependent manner.
Reduced EGFR and JAK2 levels in a concentration-dependent manner.

Cell Proliferation Assay[3]

Cell Line: MCF-7 cells
Concentration: 1.25, 2.5, 5, 10 and 20 μM
Incubation Time: 24 h
Result: Resulted in a remarkable decrease in MCF-7 cell colony number.
Almost completely inhibited colony formation by MCF-7 cells at 20 μM.

Cell Proliferation Assay[4]

Cell Line: SGC-7901 and MKN-45 cells
Concentration: 0, 2.5, 10, 20, and 40 μM
Incubation Time: 0,24, 48, and 72 h
Result: Inhibited the proliferation of SGC-7901 cells in a dose-dependent manner.
Suppressed the proliferation of SGC-7901 cells at 10 μM in a time-dependent manner.
Inhibited MKN-45 cell growth in a dose- and time-dependent manner.

Apoptosis Analysis[1]

Cell Line: A549 cells
Concentration: 0, 2, 5, 7 and 10 μM
Incubation Time: 4 and12 h
Result: Remarkably increased early apoptotic cell fractions in a concentration-dependent manner in A549 cells.
Increased caspase 3/7 activities by approximately 53 times at 10 μM after 5 h in A549 cells.
Increased the expression of cleaved PARP in A549 cells.

Apoptosis Analysis[3]

Cell Line: MCF-7 cells
Concentration: 2.5, 5, 10 and 20 μM
Incubation Time: 0, 4, 8, 20 and 24 h
Result: Induced MCF-7 cells apoptosis, with nuclear condensation and fragmentation.
Resulted DNA diffuse fragmentation in MCF-7 cells.
Decreased antiapoptotic proteins Bcl-2 and Bcl-XL, and increased proapoptotic proteins BAX and BAK in MCF-7 cells.
Increased cleaved PARP, cleaved caspase-3, and caspase-9 levels in MCF-7 cells.
Decreased MMP levels in a time-dependent manner.

Cell Autophagy Assay[1]

Cell Line: A549 cells
Concentration: 0, 2.5, 5 and 10 μM
Incubation Time: 0, 1, 3, 6, 12 and 24 h
Result: Dramatically increased the expression of LC3II in a time-dependent manner.
Decreased the expression of p-AKT (Ser473), p-AKT (Thr308), and p-mTOR (Ser2448) without affecting p62.
Resulted in the accumulation of autophagic vacuoles and increased autolysosomes.

Cell Cycle Analysis[3]

Cell Line: MCF-7 cells
Concentration: 2.5, 5 and 10 μM
Incubation Time: 24 h
Result: Showed a significant increase in the proportion of G1 phase cells in comparison with the control group at 10 μM.

Cell Cycle Analysis[4]

Cell Line: SGC-7901 and MKN-45 cells
Concentration: 0, 2.5, 5, 10, 20 and 40 μM
Incubation Time: 24 h
Result: Arrested SGC-7901 cells in the G1/G0 phase of the cell cycle in a dose-dependent manner.
Markedly increased the proportion of SGC-7901 cells in the G1/G0 phase from 47.9% to 65.7% at 10 μM.
Decreased proportion of cells in the S and G2/M phases at 10 μM.
Increased the SGC-7901 cell number in the sub-G1 phase significantly at 10 μM.
Induced cell cycle arrest in the G1/G0 phase in MKN-45 cells and increased cell proportion in the sub-G1 phase of cell cycle at higher concentration.

Apoptosis Analysis[4]

Cell Line: SGC-7901 and MKN-45 cells
Concentration: 0, 2.5, 5, 10, 20 and 40 μM
Incubation Time: 24 h
Result: Significantly increased SGC-7901 apoptosis percentage from 3.8% to 44.2% in a concentration-dependent manner.
showed apoptosis-inducing effects even at 2.5 and 5 μM.
Remarkably increased apoptotic cell number at higher concentration (40 μM).
Significantly upregulated the expression of cleaved caspase-9 and PARP in MKN-45 and SGC-7901 cells.
Promoted MKN-45 cell apoptosis in a dose-dependent manner.
In Vivo

Isocryptotanshinone (20 mg/kg, i.p., every other day for 4 weeks) inhibits SGC-7901 xenograft tumor growth in BALB/c nude mice[4].

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

Animal Model: Male BALB/c nude mice (4 weeks old) subcutaneously injected with SGC-7901 cells[4]
Dosage: 20 mg/kg
Administration: i.p., every other day for 4 weeks
Result: Significantly inhibited tumor growth compared to control.
Suppressed the phosphorylation of STAT3 in SGC-7901 tumor.
Molecular Weight

296.36

Formula

C19H20O3
CAS No.
Appearance

Solid

Color

Pink to red

SMILES

O=C1C2=C(C3=C(C=C2)C(C)(C)CCC3)C(C4=C1[C@H](C)CO4)=O
Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.
Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Purity & Documentation

Purity: 98%

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COA (252 KB)

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Keywords:

Isocryptotanshinone22550-15-8STATPhosphataseApoptosisAutophagyp38 MAPKEGFRJAKBcl-2 FamilySurvivinAktmTORPARPCaspaseAtg8/LC3CDKEpidermal growth factor receptorErbB-1HER1Janus kinasePKBProtein kinase BMammalian target of Rapamycinpoly ADP ribose polymerase Autophagy-related 8Cyclin dependent kinaseSTAT3PTP1BMAPKGClung cancerbreast cancerA549SGC-7901MKN-45MCF-795D cellsInhibitorinhibitorinhibit

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