Terephthalic acid can be used to create mice tumor models in animal modeling.

Absorption, Distribution and Excretion
... The concentrations of urine terephthalic acid(TPA) in rats after single oral administration in dose of 100 mg/kg bw were determined by high pressure liquid chromatography. ... The results showed that the first-order kinetics and two-compartment model were noted on the elimination of TPA. ... The excretion rates of TPA in urine were about 50%, 52% and 53% in 0-24 hr, 0-48 hr and 0-72 hr respectively after administration. TPA is well absorbed when given orally and rapidly eliminated via urine. Urine TPA at the end of work shift should be considered as a biomarker of exposure for the occupational workers.
Terephthalic acid is absorbed from the gastrointestinal tract and is excreted in the urine apparently unchanged. Dermal or ocular absorption is negligible.
The pharmacokinetics of (14)C terephthalic acid were determined in Fischer-344 rats after iv and oral administration. After iv injection, the plasma concentration-time data were fitted with a three-compartment pharmacokinetic model. The average terminal half-life in 3 rats was 1.2 + or - 0.4 hr, and the average volume of distribution in the terminal phase was 1.3 + or - 0.3 l/kg. Following administration by gavage, a longer terminal half-life was obtained, indicating that dissolution of (14)C TPA or absorption from the gut may have been partially rate limiting. Recovery of (14)C TPA in the urine following a bolus iv dose was 101 + or - 8%, indicating essentially complete urinary excretion of the compound. No evidence of metabolism of (14)C TPA was obtained by analysis of urine by high-performance liquid chromatography. (14)C TPA was transported to the fetus after administration of the compound to pregnant rats; the concentrations in fetal tissues were low relative to the corresponding maternal tissues. Neonatal rats exposed to 5% TPA in the diet of their dams did not develop calculi until the onset of self-feeding. TPA was rapidly excreted into urine after administration to rats, and excretory mechanisms in the dam provided an effective mechanism of defense against TPA-induced urolithiasis in neonatal rats.
By use of the Sperber in vivo chicken preparation method, infusion of radiolabeled terephthalic acid ([14C]TPA) into the renal portal circulation revealed a first-pass excretion of the unchanged compound into the urine. This model was utilized further to characterize the excretory transport of [14C]TPA and provide information on the structural specificity in the secretion of dicarboxylic acids. At an infusion rate of 0.4 nmol/min. 60% of the [14C]TPA which reached the kidney was directly excreted. An infusion rate of 3 or 6 mumol/min resulted in complete removal of [14C]TPA by the kidney. These results indicate that TPA is both actively secreted and actively reabsorbed when infused at 0.4 nmol/min and that active reabsorption is saturated with the infusion of TPA at higher concentrations. The secretory process was saturated with the infusion of TPA at 40 mumol/mn. The excretory transport of TPA was inhibited by the infusion of probenecid, salicylate, and m-hydroxybenzoic acid, indicating that these organic acids share the same organic anion excretory transport process. m-Hydroxybenzoic acid did not alter the simultaneously measured excretory transport of p-aminohippuric acid (PAH), suggesting that there are different systems involved in the secretion of TPA and PAH. The structural specificity for renal secretion of dicarboxylic acids was revealed by the use of o-phthalic acid and m-phthalic acid as possible inhibitors of TPA secretion. m-Phthalate, but not o-phthalate, inhibited TPA excretory transport, indicating that there is some specificity in the renal secretion of carboxy-substituted benzoic acids. TPA was actively accumulated by rat and human cadaver renal cortical slices.
(14)C-Labeled terephthalic acid may be both secreted and reabsorbed by the nephron, and when infused at 3 or 6 umol/min its excretion efficiency is comparable to that of p-aminohippuric acid and tetraethylammonium.

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Metabolism / Metabolites
A Rhodococcus species was isolated from soil by enriching for growth with dimethyl terephthalate as the sole carbon source. The organism degraded dimethyl terephthalate by hydrolysis of ester-bonds to free terephthalic acid which in turn was metabolized through protocatechuate by an ortho-cleavage pathway.
No evidence of metabolism of (14)C TPA was obtained by analysis of urine by high-performance liquid chromatography /following an iv dose to Fischer-344 rats/.

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Biological Half-Life
... The concentrations of urine terephthalic acid(TPA) in rats after single oral administration in dose of 100 mg/kg bw were determined by high pressure liquid chromatography. ... The results showed that the first-order kinetics and two-compartment model were noted on the elimination of TPA. The main toxicokinetic parameters were as follows: Ka = 0.51/hr, half-life ka = 0.488 hr, half-life alpha = 2.446 hr, time to peak = 2.160 hr, Ku = 0.143/hr, half-life beta = 31.551 hr, Xu(max) = 10.00 mg. ...
The pharmacokinetics of (14)C labeled terephthalic acid were determined in Fischer 344 rats after iv and oral administration. After iv injection, the plasma concentration-time data were fitted using a 3-compartment pharmacokinetic model. The avg terminal half-life in rats was 1.2 hr and the average volume of distribution in the terminal phase was 1.3 L/kg.
(14)C-Terephthalic acid has a short elimination half-life (approximately 60-100 minutes) in the plasma; however, the apparent half-life was longer following administration by gavage.

Interactions
INCR EFFECTIVENESS OF CERTAIN ANTIBIOTICS SUCH AS CHLORTETRACYCLINE.
... Chlorothiacide or dietary bicarbonate abolished terephthalic acid-induced urolithiasis in /male weanling Fisher 344 rats fed 4.0% terephthalic acid in diet for 2 weeks (postnatal days 28-42)/.
(14)C-labeled terephthalic acid may be both secreted and reabsorbed by the nephron, and when infused at 3 or 6 umol/min its excretion efficiency is comparable to that of p-aminohippuric acid and tetraethylammonium. Probenecid significantly inhibited the excretion of (14)C-labeled terephthalic acid. M-Hydroxybenzoic acid significantly decreased the excretion of (14)C-labeled terephthalic acid but was without any significant effect on the excretion of p-aminohippuric acid.
The joint injury actions and mechanisms of terephthalic acid (TPA), ethylene glycol (EG) and/or Dowtherm A (DOW): [SRP: a mixture of biphenyl and biphenyl oxide] on liver in rats were investigated. A subchronic toxicity study was designed by a 2(3) factorial method. Some enzymes, biochemical and morphologic indices reflecting the injury of liver were studied. The results showed that serum ALT and serum total bile acid (TBA) of rats in the combined intoxication groups were significantly higher than those in the groups with single toxic agent and control group. The results of factorial analysis showed that the joint action induced by TPA, EG and/or DOW were characterized as additive (TPA + EG), synergistic (EG + DOW), synergistic (TPA + DOW) and additive(TPA + EG + DOW) actions. The deduction was identified by morphologic observations.
To study injury of liver and kidney among the workers exposed to terephthalic acid(TPA), ethylene glycol(EG) and(or) dowtherm A(DOW), and research for early biological monitoring indexes. By using the method of occupational epidemiology, an investigation of industrial hygiene in a chemical fibre corporation was carried out and the changes of the liver and kidney functions were analyzed among the workers who had been exposed to TPA, EG, DOW.The values of serum gamma-glutamyl traspetidase(GGT) and total bile acid(TBA) in TPA + EG + DOW group men were (35.45 +/- 16.09) U/L, (10.29 +/- 6.76) umol/L respectively and the values of serum alanine transaminase(ALT) and TBA in TPA + EG + DOW group women were(30.68 +/- 8.58) U/L, (9.53 +/- 6.63) umol/L respectively, significantly higher than those in TPA, DOW and control groups(P < 0.05, P < 0.01). Compared with TPA, DOW and control groups, the values of urine N-acetyl-beta-D-glucosaminidase (NAG) and beta 2-2-microglobulim (beta 2-MG) in TPA + EG + DOW group of both men and women increased significantly(P < 0.05, P < 0.01), with (5.68 +/- 4.01) U/mmol Cr and (23.49 +/- 13.44) mg/mol Cr, and(6.68 +/- 4.68) U/mmol Cr and (22.80 +/- 13.00) mg/mol Cr, respectively. Analysis of regression indicated that both liver and renal injuries of the workers were evidently correlated with their exposure to TPA, EG and DOW after adjustment for the confounding factors such as sex, smoking, drinking, etc(P < 0.001). Based on available knowledge, it is reasonable to assume that the joint actions should be considered on the injury of liver and kidney caused by TPA, EG and(or) DOW among the workers. Serum ALT, GGT, TBA, urine NAG and beta 2-MG should be suggested as biomarkers for liver and kidney damage.

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Non-Human Toxicity Values
LD50 Mouse iv 770 mg/kg
LD50 Mouse ip 1900 mg/kg
LD50 Mouse ip 880 mg/kg
LD50 Rat ip 1210 mg/kg
For more Non-Human Toxicity Values (Complete) data for TEREPHTHALIC ACID (17 total), please visit the HSDB record page.

[1]. The induction of bladder stones by terephthalic acid, dimethyl terephthalate, and melamine (2,4,6-triamino-s-triazine) and its relevance to risk assessment. Regul Toxicol Pharmacol. 1985 Sep;5(3):294-313.

Terephthalic acid is a white powder. (NTP, 1992)
Terephthalic acid is a benzenedicarboxylic acid carrying carboxy groups at positions 1 and 4. One of three possible isomers of benzenedicarboxylic acid, the others being phthalic and isophthalic acids. It is a conjugate acid of a terephthalate(1-).
Terephthalic acid has been reported in Cassia roxburghii, Arabidopsis thaliana, and other organisms with data available.
See also: Pegoterate (monomer of); Polybutester (monomer of) ... View More ...

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Mechanism of Action
/The aim of this study was/ to investgate the metabolism of terephthalic acid (TPA) in rats and its mechanism. Metabolism was evaluated by incubating sodium terephthalate (NaTPA) with rat normal liver microsomes, or with microsomes pretreated by phenobarbital sodium, or with 3-methycholanthrene, or with diet control following a NADPH-generating system. The determination was performed by high performance liquid chromatography (HPLC), and the mutagenic activation was analyzed by umu tester strain Salmonella typhimurium NM2009. Expression of CYP4B1 mRNA was detected by RT-PCR. The amount of NaTPA (12.5-200 uL /per/ L) detected by HPLC did not decrease in microsomes induced by NADPH-generating system. Incubation of TPA (0.025-0.1 mmol /per/ L) with induced or noninduced liver microsomes in an NM2009 umu response system did not show any mutagenic activation. TPA exposure increased the expression of CYP4B 1 mRNA in rat liver, kidney, and bladder. Lack of metabolism of TPA in liver and negative genotoxic data from NM2009 study are consistent with other previous short-term tests...

C8H6O4

166.1308

166.027

100-21-0

26876-05-1

7489

White to off-white solid powder

1,51 g/cm3

392.4ºC at 760 mmHg

300 °C

260°C

1.83E-15mmHg at 25°C

1.648

1.083

2

4

2

12

169

0

KKEYFWRCBNTPAC-UHFFFAOYSA-N

InChI=1S/C8H6O4/c9-7(10)5-1-2-6(4-3-5)8(11)12/h1-4H,(H,9,10)(H,11,12)

terephthalic acid

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)

DMSO : ~20 mg/mL (~120.39 mM)

Solubility in Formulation 1: 2 mg/mL (12.04 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
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.

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Solubility in Formulation 2: ≥ 2 mg/mL (12.04 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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