Drug compounds have included stable heavy isotopes of carbon, hydrogen, and other elements, mostly as quantitative tracers while the drugs were being developed. Because deuteration may have an effect on a drug's pharmacokinetics and metabolic properties, it is a cause for concern [1].

Absorption, Distribution and Excretion
Following intravenous or oral administration, it is primarily excreted in the urine and bile. It appears to be rapidly cleared from the blood, with most being cleared within 5–7 hours after dialysis. In a study of subjects receiving hemodialysis, blood transfusions, or who had been exposed to PVC medical products, di(2-ethylhexyl) phthalate levels (μg/g wet tissue) in the following tissues were observed: brain (1.9), heart (0.5), kidneys (1.2–2.2), liver (1.5–4.6), lungs (1.4–2.2), and spleen (2.2–4.7). Di(2-ethylhexyl) phthalate levels have been reported in the heart tissue of newborns who underwent umbilical catheterization (whether alone or with concurrent blood product transfusions) compared to untreated newborns. (Infants) For more complete data on the absorption, distribution, and excretion of di(2-ethylhexyl) phthalates (67 in total), please visit the HSDB record page. Metabolites/Metabolites It is hypothesized that the teratogenic di(2-ethylhexyl) phthalate (DEHP) works by hydrolysis in vivo to 2-ethylhexanol (2-EXHO), which is further metabolized to 2-ethylhexanoic acid (2-EXHA), a proximal teratogen. Researchers conducted teratogenicity studies using Wistar rats, administering these substances on day 12 of gestation. At equimolar concentrations, DEHP showed the weakest teratogenicity, 2-ethylhexanol showed moderate teratogenicity, and 2-ethylhexanoic acid showed the strongest teratogenicity, consistent with the hypothesis. The similarity in the types of defects caused by these drugs also suggests a common teratogenic mechanism, with 2-ethylhexanoic acid being the primary teratogen.
After intravenous or oral administration, 2-ethylhexanoic acid is rapidly metabolized to derivatives of mono(2-ethylhexyl) phthalate. …
It has been reported that rats, after hydrolyzing di(2-ethylhexyl) phthalate to mono(2-ethylhexyl) phthalate, further metabolize it to di(2-ethylhexyl) phthalate, penta(2-ethylpentyl) phthalate, penta(2-ethylhexyl) phthalate, and di(2-ethylhexyl) phthalate.
Unlike rats, African green monkeys and ferrets excrete metabolites of di(2-ethylhexyl) phthalate in their urine; these metabolites are glucuronide derivatives of mono(2-ethylhexyl) phthalate. Glucuronization appears to occur at the free carboxyl group, while the 2-ethylhexyl substituent is oxidized to an alcohol. For more complete metabolite/metabolite data on di(2-ethylhexyl) phthalate (41 metabolites in total), please visit the HSDB record page. Di(2-ethylhexyl) phthalate (DEHP) is primarily absorbed through ingestion. It is hydrolyzed in the small intestine and absorbed as monoethylhexyl phthalate (MEHP) and 2-ethylhexanol, which may then be distributed to adipose tissue and the kidneys. MEHP is further metabolized through various oxidative reactions, producing more than 30 metabolites, some of which can be conjugated with glucuronic acid and excreted. The oxidation of 2-ethylhexanol primarily produces 2-ethylhexanoic acid and several keto acid derivatives. Most DEHP metabolites are excreted in the urine as glucuronide conjugates, while unmetabolized DEHP is excreted in the feces. (L181)

---

Biological Half-Life
The levels of DEHP and di(2-ethylhexyl) phthalate (MEHP) in the plasma of newborns undergoing exchange transfusion have been investigated. In one study, the half-life of MEHP was the same as that of DEHP (approximately 12 hours), indicating that the hydrolysis of DEHP is the rate-limiting metabolic step. However, in other children, the half-life of MEHP was longer than that of DEHP…
Following intravenous injection of radiolabeled DEHP, at least two radioactive elimination phases were observed in rat blood, with short half-lives (4.5–9 minutes and 22 minutes, respectively)... After 7 weeks of oral administration, the elimination phase in the liver was significantly slowed, with a half-life of 3–5 days... No accumulation of DEHP or MEHP was observed when the dose was 2.8 g/kg/day for 7 days... In long-term (5–7 weeks) feeding studies, no accumulation was also observed when the feed dose was 1 or 5 g/kg (equivalent to approximately 50 and 250 mg/kg body weight per day)...
...The mean plasma elimination half-lives of MEHP in 25, 40, and 60-day-old Sprague-Dawley rats were 3.9, 3.1, and 2.8 hours, respectively. ...
Two healthy male volunteers (aged 47 and 34) received a single dose of 30 mg di(2-ethylhexyl) phthalate (purity >99%), or 10 mg di(2-ethylhexyl) phthalate daily for four consecutive days... The estimated urinary elimination half-life was approximately 12 hours. ...
For more complete data on the biological half-lives of di(2-ethylhexyl) phthalate (9 types in total), please visit the HSDB records page.

Toxicity Summary
Identification and Uses: Di(2-ethylhexyl) phthalate (DEHP) is a colorless, oily liquid. DEHP can be present in plastics at concentrations ranging from 1% to 40% by weight and is used in consumer products such as artificial leather, raincoats, footwear, interior decoration, flooring, electrical wiring and cables, tablecloths, shower curtains, food packaging materials, and children's toys. DEHP is also used as a dielectric fluid (a non-conductive substance) in hydraulic fluids and capacitors, as well as in respirator leak detectors. DEHP is not currently registered for use in the United States, but approved pesticide uses may change periodically; therefore, it is essential to consult federal, state, and local authorities for currently approved uses. Human Exposure and Toxicity: DEHP has been found in a variety of foods, such as fish, shellfish, eggs, and cheese. Blood transfusions and other medical procedures involving plastic instruments can result in unintentional exposure to DEHP. Existing oral administration data indicate that di(2-ethylhexyl) phthalate (DEHP) is hydrolyzed in the intestine by pancreatic lipases. The generated metabolites, mono(2-ethylhexyl) phthalate and 2-ethylhexanol, are rapidly absorbed. Mono(2-ethylhexyl) phthalate has been detected in human teeth. Following oral administration, DEHP is extensively hydrolyzed in the intestines of some animals (e.g., rats), primarily distributed as mono(2-ethylhexyl) phthalate. However, in primates and humans, the degree of hydrolysis is much lower. Several other metabolites have been identified, with ω-oxidation and ω-1-oxidation being the major metabolic pathways. Significant species differences exist in DEHP metabolism; for example, the ω-oxidation pathway is less active in humans than in rats. Bile and urine are the main excretion routes. DEHP metabolites do not cause peroxisome proliferation in cultured human hepatocytes. Information regarding the effects of DEHP on humans is currently very limited. Two subjects reported mild gastrointestinal upset, but no other adverse reactions were observed. Adolescents exposed to high levels of di(2-ethylhexyl) phthalate (DEHP) during neonatal period showed no significant adverse effects on physical development and puberty maturation. Thyroid, liver, kidney, and male and female gonadal functions were within the normal range for their respective age and sex distributions. Animal studies: Long-term studies have found that animals treated with DEHP exhibited hepatomegaly, increased relative kidney weight, and anterior pituitary cell hypertrophy. Multiple studies have shown testicular atrophy. Young rats appear to be more susceptible than adult rats, and rats and mice appear to be more susceptible than marmosets and hamsters. The atrophy has been observed to be reversible. Both DEHP and monoethylhexyl phthalate (MONHE) are teratogenic. Most studies showed negative results for mutagenicity tests and related endpoints. DEHP may induce cell transformation and has been shown to be carcinogenic in rats and mice. The incidence of hepatocellular carcinoma increased dose-dependently in both male and female individuals of both species. The induction of hepatic peroxisome proliferation and cell replication is closely associated with the hepatocarcinogenic effects of certain non-genotoxic carcinogens, including di(2-ethylhexyl) phthalate (DEHP). However, significant differences exist in DEHP-induced peroxisome proliferation among different animal species. Ecotoxicity studies: Although few studies have been reported, DEHP appears to have low acute toxicity to algae, plants, and birds. Monoethylhexyl phthalate (MEHP), one of the major metabolites of DEHP, induces peroxisome proliferation by activating peroxisome proliferator-activated receptors (PPARs). This is thought to increase hydrogen peroxide production by peroxisomes and promote cell proliferation, leading to hepatotoxicity and carcinogenicity. MEHP is also thought to exhibit testicular toxicity by targeting and damaging testicular Sertoli cells. DEHP may exert anti-androgenic effects at critical stages of reproductive tract differentiation, reducing testosterone levels in fetal males and thus hindering development. (L181, A106)

---

Toxicity Data
LD50: 33.9 g/kg (oral, rabbit) (T33)
LD50: 10 g/kg (dermal, guinea pig) (T33)
LD50: 30.7 g/kg (intraperitoneal, rat) (T33)

---

Interactions
In studying the effects of DEHP intake on ethanol metabolism, there was a significant difference between a single dose of 1500-7500 mg/kg DEHP and continuous intake of the same dose over 7 days… 18 hours after a single DEHP administration, intraperitoneal ethanol administration appeared to reduce ethanol metabolism, as evidenced by prolonged ethanol-induced sleep time and inhibited hepatic alcohol dehydrogenase activity in the exposed rats. On the other hand, if DEHP was administered 7 days prior to ethanol administration, ethanol-induced sleep time was shortened, and the activities of both ethanol and aldehyde dehydrogenases were increased. This indicates that the change in sleep duration is due to a faster metabolic clearance of ethanol in rats repeatedly given DEHP, compared to a slower metabolic clearance in rats given a single dose. One hypothesis is that altered zinc homeostasis is the cause of teratogenicity following DEHP exposure. On day 9 of gestation (GD 9, i.e., 9 days after mating), CD-1 mice were administered corn oil (carrier) or 800 mg/kg body weight of DEHP via gavage. 3.0–4.5 hours after exposure to di(2-ethylhexyl) phthalate (DEHP), the expression levels of metallothionein (MT)-I and MT-II (two enzymes that chelate hepatic zinc and lower blood zinc levels) in the maternal liver increased, subsequently returning to baseline levels 6 hours after exposure. The expression level of zinc transporter-1 (ZnT-1, a transmembrane protein involved in zinc efflux) in the maternal liver was not affected by DEHP exposure. Three to six hours after DEHP exposure, the expression levels of MT-I, MT-II, and ZnT-1 in the embryonic brain were downregulated. The visceral yolk sac was unaffected. In a dose-response study, pregnant mice were administered DEHP by gavage at doses of 0, 50, 200, or 800 mg/kg body weight on day 9 of gestation (GD 9). Maternal mice were sacrificed three hours after exposure, and maternal liver and embryonic brain tissue were collected. …Upregulation of MT-I expression in the maternal liver reached statistical significance at a DEHP dose of 200 mg/kg body weight/day…Upregulation of MT-II expression reached statistical significance at a dose of 800 mg/kg body weight. …In the embryonic brain, the expression of MT-I and ZnT-1 was significantly reduced at a dose of 200 mg/kg body weight, and the expression of MT-II was significantly reduced at a dose of 50 mg/kg body weight. …The study concludes that maternal exposure to DEHP during organogenesis alters the expression of key fetal enzymes involved in zinc homeostasis. …Four-week-old F344 rats…after stimulation with diethylstilbestrol or pregnant mare serum gonadotropin (PMSG), the ovaries were removed and granulosa cells were collected. Cells were cultured in a medium containing 500 nM testosterone and 200 ng/mL FSH. MEHP was added to the medium and the cells were cultured for 48 hours…Comparison with other phthalate monoesters showed that the addition of 100 or 200 μM MEHP (27.8 or 55.6 mg/L) reduced estradiol levels in the medium (protein levels controlled), but this was not observed with the addition of the same molar concentrations of monomethyl phthalate, monoethyl phthalate, monopropyl phthalate, monobutyl phthalate, monoamyl phthalate, or monohexyl phthalate. Monoamyl phthalate at a concentration of 400 μM was associated with reduced estradiol production. After culturing in media supplemented with 0, 25, 50, or 100 μM MEHP (0, 7.0, 13.9, or 27.8 mg/L), the aromatase mRNA levels were determined. The graphs show that both estradiol concentration and aromatase mRNA levels decreased in a concentration-dependent manner; compared to the control group, estradiol levels at 100 μM and aromatase mRNA levels at 50 μM and 100 μM were statistically significant. The peroxisome proliferator Wy-14,643 also reduced estradiol and aromatase mRNA levels. Cholesterol side-chain lyase was unaffected by MEHP… MEHP reduced aromatase protein levels at concentrations of 100 μM and 200 μM (27.8 mg/L and 55.6 mg/L). In the final experiment, granulosa cells were incubated with 0 μM or 200 μM (0 mg/L or 56 mg/L) MEHP for 48 hours, with 8-bromocyclic adenosine monophosphate (8-Br-cAMP) added during the last 24 hours. In the absence of MEHP, 8-Br-cAMP increased the mRNA levels of aromatase and cholesterol side-chain lyase, as well as intermediate progesterone levels. In the presence of MEHP, the mRNA levels of aromatase and intermediate estradiol were inhibited, but the mRNA levels of P450 side-chain lyase and progesterone levels were not inhibited. …These results were interpreted as MEHP's transcriptional repression of aromatase being independent of the FSH-cAMP pathway. …The peroxisome proliferator-activated receptor (PPAR) pathway is considered a candidate mechanism by which MEHP inhibits steroid production in granulosa cells. …Granular cells were collected from 4-week-old Fisher rats 24 hours after injection of pregnant mare serum gonadotropin (PMSG). Cells were cultured for 48 hours in medium containing 500 nM testosterone and 200 ng/mL FSH, with or without MEHP (50 μM, 13.9 mg/L). …Compared to the control group, MEHP treatment reduced aromatase mRNA levels by more than 40%. The reduction in aromatase mRNA levels was partially reversed by the addition of a peroxisome proliferator-activated receptor (PPAR)-γ antagonist. The reduction in aromatase mRNA levels by PPAR-α and PPAR-γ agonists was similar to that after MEHP treatment. To verify whether MEHP activation of PPAR-γ and retinoic acid X receptor (RXR) leads to PPAR-γ:RXR heterodimer-mediated aromatase inhibition, we treated cells with MEHP in combination with RXR or RAR ligands. All treatments reduced aromatase levels, with significantly enhanced inhibition when MEHP was combined with 9-cis-retinoic acid. To demonstrate that MEHP activity may be mediated through PPAR-α, studies showed that MEHP treatment increased the mRNA level of 17β-hydroxysteroid dehydrogenase IV, which is induced by PPAR-α. The induction of 17β-hydroxysteroid dehydrogenase IV by MEHP was not altered upon the addition of a PPAR-γ antagonist, suggesting that MEHP activates the α isoform of PPAR. Both MEHP and selective PPAR-α agonists (not selective PPAR-γ agonists) increased the expression of Ah receptor, CYP1B1, and epoxide hydrolase. Neither MEHP nor any PPAR isoform agonist induced the expression of cholesterol side-chain lyase. Both MEHP and each specific PPAR isoform agonist induced the expression of heart-type fatty acid-binding protein (H-FABP). The conclusion is that the effect of MEHP on granulocyte gene expression (and thus reduced estrogen production) is mediated through the PPAR pathway. MEHP
For more complete data on interactions of di(2-ethylhexyl) phthalate (21 items in total), please visit the HSDB record page.

---

Non-human toxicity values
Rats oral LD50 >25 g/kg
Rats intravenous LD50 250 mg/kg
Mice oral LD50 >30 g/kg
Mice intraperitoneal LD50 14 g/kg
For more complete data on non-human toxicity of di(2-ethylhexyl) phthalate (10 items in total), please visit the HSDB record page.

[1]. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019 Feb;53(2):211-216.

Di(2-ethylhexyl) phthalate (DEHP) is a synthetic chemical commonly added to plastics to increase their flexibility. DEHP is a colorless liquid and almost odorless. It is found in a wide variety of plastic products, such as wallpaper, tablecloths, floor tiles, furniture upholstery, shower curtains, garden hoses, swimming pool liners, raincoats, baby pants, dolls, certain toys, shoes, car interiors and headliners, packaging films and sheets, wire and cable sheathing, medical catheters, and blood bags. According to an independent committee of scientific and health experts, DEHP may be carcinogenic. It may also cause developmental toxicity and male reproductive toxicity, according to the National Institute for Occupational Safety and Health (NIOSH) and the Food and Drug Administration (FDA). Di(2-ethylhexyl) phthalate is a colorless to pale yellow oily liquid and is almost odorless. (US Coast Guard, 1999)
Di(2-ethylhexyl) phthalate is a phthalate ester, a di(2-ethylhexyl) ester of phenyl-1,2-dicarboxylic acid. It has functions as an inhibitor of apoptosis, an androstane receptor agonist, and a plasticizer. It is a phthalate ester and diester.
Di(2-ethylhexyl) phthalate has been reported to be found in Penicillium olsenii, Streptomyces, and other organisms with relevant data.
Di(2-ethylhexyl) phthalate is a colorless, oily organic carcinogen with a slight odor. Di(2-ethylhexyl) phthalate is primarily used as a plasticizer in the manufacture of flexible materials for many household products. Inhalation, ingestion, and skin contact are its main potential routes of exposure. Animal studies have shown that exposure to di(2-ethylhexyl) phthalate is associated with an increased incidence of hepatocellular carcinoma. This substance is reasonably expected to be a human carcinogen. (NCI05)
Di(2-ethylhexyl) phthalate (DEHP) is a synthetic chemical commonly added to plastics to increase their flexibility. Exposure to DEHP is generally low and harmless, but increased exposure through intravenous fluid infusion via plastic tubing or ingestion of contaminated food or water can have toxic effects. This is particularly concerning because DEHP is known to leach into liquids that come into contact with DEHP-containing plastics. (L181, L182)
Phytrates. These are light-colored, odorless liquids used as plasticizers in a variety of resins and elastomers.

---

Mechanism of Action
…1000 mg/kg body weight of MEHP (purity >97%) was dissolved in corn oil and administered by gavage to 5-week-old Sprague-Dawley rats, 28-day-old wild-type C57CL/6 mice, or 28-day-old gld mice. GLD mice express a dysfunctional fasL protein that fails to bind to the fas receptor to initiate apoptosis. Following MEHP exposure, apoptosis primarily occurred in spermatocytes in both wild-type and GLD mice. In wild-type mice, germ cell apoptosis significantly increased 6 to 48 hours after MEHP exposure. Apoptotic activity peaked between 12 and 24 hours, representing a 5-fold increase from baseline. In GLD mice, apoptotic levels were approximately 2-fold higher than baseline at 12 and 48 hours after MEHP exposure. Apoptotic activity returned to baseline levels in both groups at 96 hours post-exposure. Western blot analysis showed that fas expression was significantly increased (approximately 3-fold) 3 hours after MEHP exposure in wild-type mice. In GLD mice, fas expression did not change significantly after MEHP exposure. DR4, DR5, and DR6 proteins (fas-independent death receptors in the tumor necrosis factor (TNF) superfamily) were expressed in both wild-type and gld mice, but MEHP exposure did not increase the expression of DR4, DR5, and DR6 proteins in either strain. In the testes of Sprague-Dawley rats, DR5 expression was significantly increased (approximately 1.5-fold) at 1.5 and 3 hours after MEHP exposure, while DR4 expression remained largely unchanged. The precursor caspase 8 cleavage product, a downstream receptor-mediated signaling molecule of the apoptosis pathway, was detected in the testes of both wild-type and gld mice, but its expression was significantly increased only 6 hours after MEHP exposure in gld mice. Electrophoretic mobility shift analysis indicated that DNA binding of NF-κB (a receptor-mediated downstream signaling molecule that may be involved in cell death or survival) was generally reduced in wild-type mice, but NF-κB expression was upregulated in gld mice after MEHP exposure. The conclusion is that these findings suggest that germ cell-associated death receptors and their downstream signaling products appear to respond to MEHP-induced cell damage. Sprague-Dawley male rats were orally administered 250, 500, or 750 mg/kg/day of di(2-ethylhexyl) phthalate (DEHP) for 28 days, while control rats were given corn oil. Western blotting was used to analyze the levels of cell cycle regulators (pRb, cyclins, CDK, and p21) and apoptosis-related proteins. The roles of peroxisome proliferator-activated receptor γ (PPAR-γ), scavenger receptor type B 1 (SR-B1), and ERK1/2 were further investigated to explore the signaling pathways of DEHP-induced apoptosis. The results showed that in rats treated with 500 and 750 mg/kg/d DEHP, the levels of pRB, cyclin D, CDK2, cyclin E, and CDK4 were significantly decreased, while the level of p21 was significantly increased. DEHP exposure led to a dose-dependent increase in the expression of PPAR-γ and RXRα proteins in the testes, while significantly decreasing the expression of RXRγ protein. In addition to PPAR-γ, DEHP also significantly increased the levels of SR-B1 mRNA and phosphorylated ERK1/2 protein. Furthermore, DEHP treatment induced the cleavage of pro-caspase-3 and its substrate, poly(ADP-ribose) polymerase (PARP), in a dose-dependent manner. These data suggest that DEHP exposure may induce the expression of apoptosis-related genes in the testes by inducing PPAR-γ and activating the ERK1/2 pathway. This study employed genome-wide expression profiling combined with gene ontology (GO) and pathway mapping tools to identify affected molecular pathways and processes, and to investigate the acute effects of a non-genotoxic carcinogen and the peroxisome proliferator (PP) dioctyl phthalate (DEHP) in mouse liver (as a model system). Consistent with the known mechanisms of DEHP action, GO analysis of transcriptomic profiling data revealed significant overexpression of genes associated with peroxisome cellular components and those involved in carboxylic acid and lipid metabolism. Furthermore, the study revealed changes in gene expression related to other biological functions such as complement activation, hemostasis, endoplasmic reticulum overload response, and circadian rhythms. These data collectively reveal potential new pathways of action of the peroxisome proliferator-activated receptor (PP) and provide new insights into the mechanisms by which non-genotoxic carcinogens control hepatocyte hypertrophy and proliferation. Peroxisome proliferator-activated receptor α (PPAR-α) is a nuclear receptor belonging to the steroid hormone receptor superfamily; it forms a heterodimer with the retinol X receptor (RXR) and binds to DNA. Peroxisome proliferator response elements (PPREs) have been found in genes of both peroxisomes and microsomal fatty acid oxidases. …Species-specific differences in responses to peroxisome proliferators (e.g., dioctyl phthalate, DEHP), particularly between humans and rats and mice, may be attributed to…PPAR-α expression levels and function, the presence of active PPREs in specific gene promoter regions, and other aspects of interactions with transcriptional regulatory proteins. …Significant species differences exist in PPAR-α mRNA expression in rodent and human livers, with the latter expressing only 1–10% of the levels found in mouse or rat livers. …PPAR-α protein expression levels in human livers are less than 10% of those in mice. …In most human samples studied, PPREs were found to bind primarily to other competing proteins that may block the response to peroxisome proliferators. Furthermore, the levels of PPAR-α protein detected in human livers are lower than estimated by RNA analysis, which can be explained by the finding that a significant portion of PPAR-α mRNA in human livers is missplicing. In 10 human liver samples, truncated PPAR-α mRNA accounted for 25-50% of total PPAR-α mRNA, while no truncated PPAR-α mRNA was detected in rat and mouse livers. The truncated human PPAR-α mRNA expressed in vitro exhibited the following two characteristics: (a) it could not bind to PPRE, a necessary step for gene activation; and (b) it interfered with the gene activation of full-length human PPAR-α, partly because it reduced the level of the coactivator CREB-binding protein, another important component of transcriptional regulation. …The differences in sensitivity to peroxisome proliferators among different species may depend on gene-specific factors. For example, the PPRE promoter region required for transcriptional activation of rodent genes is not present in the promoter regions of human genes… The human liver does not respond significantly to peroxisome proliferation and hepatocyte proliferation induction, which can be explained by multiple aspects of PPAR-α-mediated gene expression regulation… In summary, these findings suggest that the increased incidence of liver tumors in mice and rats treated with di(2-ethylhexyl) phthalate (DEHP) is caused by a mechanism that does not exist in humans.

C24D38O4

428.79

428.515

352431-42-6

DEHP;117-81-7

8343

Colorless to light yellow liquid

1.0±0.1 g/cm3

384.9±10.0 °C at 760 mmHg

-58 °F (NTP, 1992)
-55 °C
-50 °C
-58 °F
-58 °F

207.2±0.0 °C

0.0±0.9 mmHg at 25°C

1.489

8.71

0

4

16

28

394

0

C1(=C([2H])C(C(OC([2H])([2H])C([2H])(C([2H])([2H])C([2H])([2H])[2H])C([2H])([2H])C([2H])([2H])C([2H])([2H])C([2H])([2H])[2H])=O)=C(C(OC([2H])([2H])C([2H])(C([2H])([2H])C([2H])([2H])[2H])C([2H])([2H])C([2H])([2H])C([2H])([2H])C([2H])([2H])[2H])=O)C([2H])=C1[2H])[2H]

BJQHLKABXJIVAM-UHFFFAOYSA-N

InChI=1S/C24H38O4/c1-5-9-13-19(7-3)17-27-23(25)21-15-11-12-16-22(21)24(26)28-18-20(8-4)14-10-6-2/h11-12,15-16,19-20H,5-10,13-14,17-18H2,1-4H3

bis(2-ethylhexyl) benzene-1,2-dicarboxylate

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.

---

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).

View More

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)

---

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).

View More

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

---

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.

---

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