2. Apoptosis Epigenetics Cell Cycle/DNA Damage
  3. Apoptosis Caspase PARP
  4. Isoegomaketone

Isoegomaketone is an orally active apoptosis inducer and radiosensitizer. Isoegomaketone regulates multiple key signaling pathways such as PI3K/AKT/mTOR, NF-κB, MAPK, cleaves Caspase family proteins and PARP, and modulates Bax, AIF and endoplasmic reticulum stress proteins. Isoegomaketone also induces autophagy and keratinocyte proliferation, effectively reduces the levels of inflammatory factors and oxidative stress, inhibits adipocyte differentiation, and resensitizes TRAIL-resistant cancer cells. Isoegomaketone can be applied to research related to colorectal cancer, melanoma, lung cancer, prostate cancer, liver cancer, as well as rheumatoid arthritis and obesity.

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Isoegomaketone

Isoegomaketone Chemical Structure

CAS No. : 34348-59-9

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Isoegomaketone Related Antibodies

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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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PARP PARP1 PARP2 PARP3 PARP4 TNKS1/PARP5A TNKS2/PARP5B PARP7 PARP10 PARP14 PARP15 PARP12 PARP16

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Description

Isoegomaketone is an orally active apoptosis inducer and radiosensitizer. Isoegomaketone regulates multiple key signaling pathways such as PI3K/AKT/mTOR, NF-κB, MAPK, cleaves Caspase family proteins and PARP, and modulates Bax, AIF and endoplasmic reticulum stress proteins. Isoegomaketone also induces autophagy and keratinocyte proliferation, effectively reduces the levels of inflammatory factors and oxidative stress, inhibits adipocyte differentiation, and resensitizes TRAIL-resistant cancer cells. Isoegomaketone can be applied to research related to colorectal cancer, melanoma, lung cancer, prostate cancer, liver cancer, as well as rheumatoid arthritis and obesity[1][2][3][4].

In Vitro

Isoegomaketone (10-100 μM) potently induces apoptosis in human colorectal adenocarcinoma DLD1 cells via the mitochondria-dependent cytochrome c and AIF pathways, with an IC50 of approximately 25 μM[1].
Isoegomaketone (10 μM; 24 h) significantly promotes the proliferation and migration of human keratinocyte HaCaT cells by activating the MAPK/ERK pathway[1].
Isoegomaketone (25-50 μM; 24 h) induces the translocation of apoptosis-inducing factor (AIF) from mitochondria to the nucleus in human colon cancer DLD1 cells[2].
Combination treatment with Isoegomaketone (100 µg/mL) and 8 Gy radiotherapy significantly reduces the expression of HIF-1α and the phosphorylation levels of PI3K and AKT in HT-29 colon cancer cells, compared with monotherapy[3].
Combination treatment with Isoegomaketone (100 µg/mL) and 8 Gy radiotherapy significantly enhances apoptosis (via upregulating BAX expression and downregulating BCL-2 expression) and autophagy (via upregulating Beclin-1 expression and promoting the conversion of LC3 I to LC3 II) in HT-29 colon cancer cells, compared with monotherapy[3].

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

Isoegomaketone Related Antibodies

Apoptosis Analysis[2]

Cell Line: human colon cancer DLD1 cells
Concentration: 10 μM, 25 μM, 50 μM, 100 μM
Incubation Time: 24 h
Result: Induced apoptosis in ~20% of DLD1 cells at 50 μM.
Induced apoptosis in ~70% of DLD1 cells at 100 μM.
Triggered cleavage of PARP, producing the characteristic 85 kDa cleaved fragment alongside the full-length 116 kDa protein at 50 μM.

Western Blot Analysis[2]

Cell Line: human colon cancer DLD1 cells
Concentration: 25 μM, 50 μM
Incubation Time: 24 h
Result: Caused dose-dependent release of cytochrome c from mitochondria to cytosol, with reduced mitochondrial cytochrome c levels and increased cytosolic cytochrome c levels at 25 μM and 50 μM.
Induced dose-dependent Bid cleavage, shown by reduced full-length Bid levels at 25 μM and 50 μM.
Promoted Bax translocation from cytosol to mitochondria, shown by reduced cytosolic Bax levels and increased mitochondrial Bax levels at 25 μM and 50 μM.\nInduced dose-dependent translocation of AIF, with decreased AIF levels in mitochondrial fractions, transiently increased levels in cytosolic fractions, and increased levels in nuclear fractions at 25 μM and 50 μM.
In Vivo

Isoegomaketone (5-20 mg/kg) significantly inhibits the growth of melanoma volume in B16-bearing mice[1].
Isoegomaketone (10 mg/kg; p.o.; once daily; for 7 consecutive days) significantly reduces arthritis severity, hind paw inflammatory responses, ankle joint pathological damage, and NLR levels in collagen antibody-induced rheumatoid arthritis BALB/c mice[1].
Isoegomaketone (10 mg/kg; daily) significantly reduces body weight gain and visceral fat accumulation by 45% in high-fat diet-induced obese C57BL/6J mice[1].
Combination of Isoegomaketone (100 mg/kg; i.p.; once daily; for 14 consecutive days) with daily 8 Gy radiotherapy achieves complete tumor eradication and 100% survival rate in HT-29 colon cancer xenograft mice, while alleviating radiotherapy-induced intestinal injury by regulating cell apoptosis, autophagy and the PI3K/AKT/mTOR signaling pathway[3].
Isoegomaketone (5-10 mg/kg/day; oral administration; once daily; for 4 consecutive days) dose-dependently alleviates collagen antibody-induced rheumatoid arthritis in male BALB/c mice[4].

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

Animal Model: BALB/c nude (male, 4 weeks-old, weight 18~22 g, HT-29 human colon cancer cells xenograft)[3]
Dosage: 100 mg/kg; 8 Gy (daily X-ray radiotherapy)
Administration: i.p.; daily; 14 days
Result: Achieved almost complete elimination of xenograft tumors with no recurrence observed over the treatment period.
Resulted in a 100% mouse survival rate over 14 days, compared to 40-60% survival with either monotherapy and 0% survival in controls.
Significantly upregulated BAX expression and downregulated BCL-2 expression in tumor tissue.
Enhanced the conversion of LC3 I to LC3 II and upregulated Beclin-1 expression to a greater extent than monotherapy.
Increased peripheral blood levels of white blood cells, neutrophils, and monocytes compared to monotherapy or control groups.
Reduced radiation-induced malondialdehyde levels in intestinal tissue.
Increased glutathione and catalase activities in intestinal tissue compared to radiotherapy alone.
Decreased levels of TNF-α, NF-κB, and IL-1β in intestinal tissue compared to radiotherapy alone.
Reversed radiotherapy-induced increases in γH2AX expression and phosphorylation of PI3K, AKT, and mTOR in intestinal tissue.
Improved histopathological damage to intestinal villi.
Animal Model: BALB/c (male, 5 weeks old, collagen antibody-induced arthritis model)[4]
Dosage: 5 mg/kg/day; 10 mg/kg/day
Administration: p.o.; once daily; 4 days (days 3-6)
Result: Reduced arthritic score by 73%, paw volume by 15%, and paw thickness by 14% at day 7 (10 mg/kg/day dose).
Lowered neutrophil-to-lymphocyte ratio by 85% at day 7 (10 mg/kg/day dose).
Decreased mean histopathological arthritic score to 1.17 (10 mg/kg/day dose).
Significantly reduced paw volume by 9.5% (day 5), 17.4% (day 6), and 13.7% (day 7) (10 mg/kg/day dose).
Significantly reduced paw thickness by 15.8% (day 6) and 14.2% (day 7) (10 mg/kg/day dose).
Attenuated arthritic signs from days 5 through 7 and delayed disease onset compared to apigenin-treated controls (10 mg/kg/day dose).
Reduced synovial hyperplasia and inflammatory cell infiltration in joint spaces (10 mg/kg/day dose).
Resulted in mean histopathological arthritic score of 2.83 (5 mg/kg/day dose).
Showed no significant reductions in paw volume, paw thickness, arthritic score, or neutrophil-to-lymphocyte ratio compared to control CAIA mice (5 mg/kg/day dose).
Molecular Weight

164.20

Formula

C10H12O2
CAS No.
Appearance

Liquid (Density: 1.003±0.06 g/cm3)

Color

Colorless to light yellow

SMILES

CC(C)/C=C/C(C1=COC=C1)=O
Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.
Storage
Pure form -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Purity & Documentation
References
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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Isoegomaketone34348-59-9ApoptosisCaspasePARPpoly ADP ribose polymeraseB16 mouse melanoma cellsSTAT-1MAPK/ERKPI3K/AKT/mTORNrf2HIF-1αDLD1 human colorectal adenocarcinoma cellsNF-κBAP-1p38-MAPKInhibitorinhibitorinhibit

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