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[1][3][4]. 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].

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 p38α p38β MAPK13 p38δ p38γ

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Caspase 1 Caspase 2 Caspase 3 Caspase 4 Caspase 5 Caspase 6 Caspase 7 Caspase 8 Caspase 9 Caspase 10 Caspase 12 Caspase Caspase 11 Caspase-13

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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[1][3][4]. Isocryptotanshinone suppresses the xenograft gastric cancer (GC) tumor growth in BALB/c nude mice[3]. 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: ≥98.0%

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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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