Isopentenone (10-100 μM) effectively induced apoptosis in human colorectal adenocarcinoma DLD1 cells via mitochondrial-dependent cytochrome c and AIF pathways, with an IC50 of approximately 25 μM [1]. Isopentenone (10 μM; 24 h) significantly promoted the proliferation and migration of human keratinocytes HaCaT by activating the MAPK/ERK pathway [1]. Isopentenone (25-50 μM; 24 h) induced the translocation of apoptosis-inducing factor (AIF) from mitochondria to the nucleus in human colon cancer DLD1 cells [2]. Compared with monotherapy, disodium isopentenyl methoxycinnamate (100 µg/mL) combined with 8 Gy radiotherapy significantly reduced the expression of HIF-1α and the phosphorylation levels of PI3K and AKT in HT-29 colon cancer cells [3]. Compared with monotherapy, disodium isopentenyl methoxycinnamate (100 µg/mL) combined with 8 Gy radiotherapy significantly enhanced apoptosis (by upregulating BAX expression and downregulating BCL-2 expression) and autophagy (by upregulating Beclin-1 expression and promoting the conversion of LC3 I to LC3 II) in HT-29 colon cancer cells [3].

Isopentenone (5-20 mg/kg) significantly inhibited the growth of melanoma volume in tumor-bearing mice (B16 mice)[1]. Isopentenone (10 mg/kg; orally; once daily for 7 days) significantly reduced the severity of arthritis, hind paw inflammation, ankle pathological damage, and neutrophil-to-lymphocyte ratio (NLR) in collagen antibody-induced rheumatoid arthritis BALB/c mice[1]. Isopentenone (10 mg/kg; once daily) significantly reduced the weight gain and visceral fat accumulation in high-fat diet-induced obese C57BL/6J mice by up to 45%[1]. Isopentenone (100 mg/kg; intraperitoneal injection; once daily for 14 days) combined with daily 8 Gy radiotherapy completely cleared tumors in HT-29 colon cancer xenograft mice with a survival rate of 100%, while also alleviating radiotherapy-induced intestinal damage by regulating apoptosis, autophagy, and the PI3K/AKT/mTOR signaling pathway[3]. Isopentenone (5-10 mg/kg/day; orally; once daily for 4 days) can dose-dependently alleviate collagen antibody-induced rheumatoid arthritis in male BALB/c mice [4].

Apoptosis analysis [2]
Cell Types: Human colon cancer DLD1 cells
Tested Concentrations: 10 μM, 25 μM, 50 μM, 100 μM
Incubation Duration: 24 hours
Experimental Results: At a concentration of 50 μM, approximately 20% of DLD1 cells were induced to apoptosis. At a concentration of 100 μM, approximately 70% of DLD1 cells were induced to apoptosis. At a concentration of 50 μM, PARP cleavage was triggered, producing a characteristic 85 kDa cleavage fragment and a full-length 116 kDa protein.

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Western Blot Analysis [2]
Cell Types: Human colon cancer DLD1 cells
Tested Concentrations: 25 μM, 50 μM
Incubation Duration: 24 hours
Experimental Results: Caused dose-dependent release of cytochrome c from mitochondria into the cytosol, with decreased mitochondrial cytochrome c levels and increased cytochrome c levels in the cytosol at concentrations of 25 μM and 50 μM. Induced dose-dependent cleavage of Bid, as evidenced by decreased full-length Bid levels at concentrations of 25 μM and 50 μM. Promoted the translocation of Bax from the cytosol to the mitochondria, as evidenced by decreased cytosol Bax levels and increased mitochondrial Bax levels (at concentrations of 25 μM and 50 μM). AIF dose-dependent translocation was induced, resulting in decreased AIF levels in the mitochondrial fraction, transiently increased AIF levels in the cytosol fraction, and increased AIF levels in the nuclear fraction (at concentrations of 25 μM and 50 μM).

Animal/Disease Models:BALB/c nude mice (male, 4 weeks old, weighing 18-22 g, xenografts of HT-29 human colon cancer cells) [3]
Doses: 100 mg/kg; 8 Gy (daily X-ray radiotherapy)
Route of Administration: Intraperitoneal injection; once daily; 14 days
Experimental Results: The xenografts were almost completely eliminated during treatment, and no recurrence was observed. After 14 days, the survival rate of mice was 100%, while the survival rate of the monotherapy group was 40-60%, and the survival rate of the control group was 0%. BAX expression was significantly upregulated and BCL-2 expression was significantly downregulated in tumor tissue. The conversion of LC3 I to LC3 II was enhanced, and the upregulation of Beclin-1 expression was higher than that of monotherapy. Compared with the monotherapy group or the control group, the levels of peripheral blood leukocytes, neutrophils and monocytes were increased. Radiation-induced malondialdehyde levels in intestinal tissue were decreased. Compared with radiotherapy alone, glutathione and catalase activities were increased in intestinal tissue. TNF-α, NF-κB, and IL-1β levels were decreased in intestinal tissue compared with radiotherapy alone. Radiotherapy-induced increases in γH2AX expression and PI3K, AKT, and mTOR phosphorylation levels in intestinal tissue were reversed. Histopathological damage to intestinal villi was improved.

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Animal/Disease Models:BALB/c (male, 5 weeks old, collagen antibody-induced arthritis model) [4]
Doses: 5 mg/kg/day; 10 mg/kg/day
Route of Administration: Oral; once daily; 4 days (days 3-6)
Experimental Results: On day 7, the arthritis score decreased by 73%, claw volume decreased by 15%, and claw thickness decreased by 14% (10 mg/kg/day). On day 7, the neutrophil-to-lymphocyte ratio decreased by 85% (10 mg/kg/day). The mean histopathological arthritis score decreased to 1.17 (10 mg/kg/day). Claw volume was significantly reduced, decreasing by 9.5% on day 5, 17.4% on day 6, and 13.7% on day 7 (10 mg/kg/day). Claw thickness was significantly reduced, decreasing by 15.8% on day 6 and 14.2% on day 7 (10 mg/kg/day). Compared with the apigenin-treated control group, this dose group alleviated arthritis symptoms and delayed disease onset from day 5 to day 7 (10 mg/kg/day). This dose group reduced synovial hyperplasia and inflammatory cell infiltration within the joint cavity (10 mg/kg/day). The mean histopathological arthritis score decreased to 2.83 (5 mg/kg/day). Compared with control CAIA mice, this dose group did not show significant reductions in claw volume, claw thickness, arthritis score, or neutrophil/lymphocyte ratio (5 mg/kg/day).

[1]. Advances in the Pharmacological Activities and Effects of Perilla Ketone and Isoegomaketone. Evid Based Complement Alternat Med. 2022;2022:8809792. Published 2022 Oct 28.

[2]. Isoegomaketone induces apoptosis through caspase-dependent and caspase-independent pathways in human DLD1 cells. Biosci Biotechnol Biochem. 2011;75(7):1306-1311.

[3]. Isoegomaketone improves radiotherapy efficacy and intestinal injury by regulating apoptosis, autophagy and PI3K/AKT/mTOR signaling in a colon cancer model. Oncol Rep. 2025;53(4):51.

[4]. Isoegomaketone Alleviates the Development of Collagen Antibody-Induced Arthritis in Male Balb/c Mice. Molecules. 2017;22(7):1209. Published 2017 Jul 19.

C10H12O2

164.20

34348-59-9

Colorless to light yellow liquid (Density: 1.003±0.06 g/cm3)

CC(C)/C=C/C(C1=COC=C1)=O

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)