| Field | Specification |
|---|---|
| Target | |
| Alternative names | DINP |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C26H42O4 |
| Purity | |
| SMILES | |
| Form | Liquid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Diisononyl phthalate (DINP) is an orally active polyvinyl chloride plasticizer and indirect food additive. It activates the ACE/AT1R axis, inhibits NO production, and reduces expression of eNOS; it induces increased blood pressure in mice and monocytic leukemia in rats, and it can be used in hypertension-related research[1][2]. It is supplied as a colorless to light yellow liquid (C26H42O4, MW 418.61) at 98.0% purity.
Physical & Chemical Properties
| CAS Number | 28553-12-0 |
|---|---|
| Molecular Formula | C26H42O4 |
| Molecular Weight | 418.61 g/mol |
| Purity | 98.0% |
| Appearance | Liquid |
| Color | Colorless to light yellow |
| Density | 0.972 g/cm3 |
| SMILES | O=C(OCCCCCCC(C)C)C1=CC=CC=C1C(OCCCCCCC(C)C)=O |
| Target | AT1 Receptor, eNOS |
| Signaling Pathway | Immunology/Inflammation; GPCR/G Protein |
| Solubility | In Vitro: DMSO: 100 mg/mL (238.89 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) |
| Storage | Store at room temperature 3 years. In solvent: -80°C, 2 years; -20°C, 1 year. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
[2]. Lington A W, et al. Chronic toxicity and carcinogenic evaluation of diisononyl phthalate in rats[J]. Fundamental and applied toxicology, 1997, 36(1): 79-89.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | 100 mg/mL (238.89 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 2 years) or -20°C (up to 1 year); avoid repeated freeze-thaw cycles.
In Vivo
Choose the formulation that suits the animal model and route of administration; percentages are volume ratios of the final working solution. Start from a clear DMSO stock (see In Vitro above), add the co-solvents one at a time in the order listed, mixing after each addition, and prepare the working solution fresh on the day of dosing. If precipitation or phase separation occurs, gentle warming or sonication can help.
Protocol 1
| Composition | 10% DMSO + 90% Corn Oil |
|---|---|
| Result | ≥ 5 mg/mL (11.94 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 5 mg/mL (saturation not determined). Use with caution if continuous dosing will exceed two weeks. For 1 mL of working solution: add 100 μL DMSO stock (50.0 mg/mL) to 900 μL corn oil. |
Data provided by the manufacturer.
In Vitro
No genotoxic activity of diisononyl phthalate is seen in bacterial or mammalian cells[2].
In Vivo
In C57/BL6 mice, daily intragastric exposure to diisononyl phthalate alone (0.15-15 mg/kg/day; 42 days) induces a dose-dependent rise in blood pressure, higher heart rate (at 15 mg/kg/day), and cardiovascular/renal tissue damage, together with upregulated ACE and AT1R expression and downregulated eNOS expression in the aorta, and reduced serum NO production[1]. In C57/BL6 mice receiving diisononyl phthalate (0.15-15 mg/kg/day; oral gavage; daily; 42 days) together with daily subcutaneous 1 mg/kg/day dexamethasone for 42 days, the hypertension, cardiovascular/renal tissue damage, and ACE/AT1R and eNOS/NO pathway dysregulation induced by dexamethasone are exacerbated dose-dependently, and this effect is reversible by treatment with an ACE inhibitor[1]. In Fischer 344 rats, dietary intake of diisononyl phthalate (DINP) at 0.03-0.6 wt% daily for 2 years induces dose-dependent increases in liver, kidney and spleen weights. In the high-dose group, male rats show a slight decrease in body weight, and both the middle- and high-dose groups show a statistically significant rise in monocytic leukemia incidence across the 2-year experimental period[2].
| Animal Model | C57/BL6 (male, 5-6 weeks old, ~20 g, specific pathogen free)[1] |
|---|---|
| Dosage | 0.15 mg/kg/day; 1.5 mg/kg/day; 15 mg/kg/day |
| Administration | p.o.; daily; 42 days |
| Result | Increased systolic blood pressure to 133 mmHg (~17.7% rise vs. saline group) at 15 mg/kg/day dose. Raised systolic, diastolic, and mean blood pressure in a dose-dependent, statistically significant manner (P < 0.01 vs. saline group). Increased heart rate in a statistically significant manner only at 15 mg/kg/day dose (P < 0.01 vs. saline group). Thickened interventricular septum, ventricular wall, and aortic wall, and induced cardiomyocyte hypertrophy in a dose-dependent, statistically significant manner (P < 0.01 vs. saline group). Induced glomerular vacuoles, hyaline degeneration, reduced glomerular size, and thickened glomerular basement membranes. Increased aortic ACE and AT1R expression in a dose-dependent, statistically significant manner (P < 0.01 vs. saline group). Decreased aortic eNOS expression in a dose-dependent, statistically significant manner (P < 0.01 vs. saline group at 15 mg/kg/day dose). Sharply decreased serum NO concentration (P < 0.01 vs. saline group). |
| Animal Model | C57/BL6 (male, 5-6 weeks old, ~20 g, specific pathogen free, hypertension induced by 1 mg/kg/day dexamethasone s.c. daily for 42 days)[1] |
|---|---|
| Dosage | 0.15 mg/kg/day; 1.5 mg/kg/day; 15 mg/kg/day |
| Administration | p.o.; daily; 42 days; co-administered with 1 mg/kg/day dexamethasone s.c.; daily; 42 days |
| Result | Aggravated dexamethasone-induced increases in systolic, diastolic, and mean blood pressure in a dose-dependent, significant manner (P < 0.01 vs. dexamethasone-only group for higher doses). Increased heart rate significantly at 15 mg/kg/day dose vs. dexamethasone-only group. Exacerbated dexamethasone-induced aortic wall thickening significantly (P < 0.01 vs. dexamethasone-only group) and glomerular damage. Increased aortic ACE and AT1R expression significantly compared to dexamethasone-only group. Decreased aortic eNOS expression in a dose-dependent, significant manner (P < 0.01 vs. dexamethasone-only group). Slightly further reduced serum NO concentration (not statistically significant vs. dexamethasone-only group). Saw alleviation of increases in blood pressure, heart rate, and tissue damage, and normalization of ACE, AT1R, and eNOS expression with ACE inhibitor treatment. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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