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Triethylenetetramine (TETA and triene), also called trientine (INN), is an organic compound with the formula [CH2NHCH2CH2NH2]2. Triethylenetetramine oily liquid is colorless, but like many amines, it acquires a yellowish color due to impurities from oxidation with air. It is soluble in polar solvents. Branched isomer tris(2-aminoethyl)amine and piperazine derivatives may also be present in commercial TETA samples.

CAS No. : 112-24-3

EC No. : 203-950-6



Triethylenetetramine (TETA)

Triethylenetetramine (TETA) Usage Areas

The reactivity and uses of triethylenetetramine (TETA) are similar to those for the related polyamines ethylenediamine and diethylenetriamine. Triethylenetetramine (TETA) is primarily used as a crosslinker ("hardener") in epoxy curing.

Medical uses of triethylenetetramine

Triethylenetetramine hydrochloride salt (TETA), called triethylenetetramine (TETA) hydrochloride, is a chelating agent used to bind and remove copper from the body to treat Wilson's disease, especially in those with penicillamine intolerance. Some recommend Triethylenetetramine (TETA) as first-line therapy, but experience with penicillamine is more extensive.

Triethylenetetramine (TETA) hydrochloride (brand name Syprine) was approved for medical use in the United States in November 1985.

Triethylenetetramine Production

Triethylenetetramine (TETA) is prepared by heating ethylenediamine or ethanolamine/ammonia mixtures over an oxide catalyst. This process yields various amines, particularly ethylene amines, which are separated by distillation and sublimation.

coordination chemistry of triethylenetetramine

Triethylenetetramine (TETA) is a tetradentate ligand called triene in coordination chemistry. Octahedral complexes of M-type (triene) L2 can adopt several diastereomeric structures.

Triethylenetetramine tetrahydrochloride (brand name Cuprior) was approved for medical use in the European Union in September 2017. Triethylenetetramine (TETA) is indicated for the treatment of Wilson's disease in D-intolerant adults, adolescents, and children aged five years and older. penicillamine therapy.

Triethylenetetramine (TETA) dihydrochloride (brand name Cufence) was approved for medical use in the European Union in July 2019. Indicated for the treatment of Wilson's disease in D-intolerant adults, adolescents, and children aged five years and older. . penicillamine therapy.

The most common side effects are nausea, skin rash, duodenitis (inflammation of the duodenum, intestinal esophagus), especially when starting treatment.

name) and severe colitis (inflammation of the large intestine that causes pain and diarrhea).

triethylenentetramine Properties

Chemical formula C6H18N4

Molar mass 146,238 g mol − 1

Appearance Colorless liquid

Smell Fish, ammonia

Density 982 mg mL − 1

melting point -34.6 ° C; -30.4°F; 238.5K

boiling point 266.6 ° C; 511.8°F; 539.7K

Solubility in water Miscible

daily P 1.985

Vapor pressure <1 Pa (at 20 °C)

refractive index (nD) 1.496


Triethylenetetramine Administration

Triethylenetetramine was used as an additive to improve the peak resolution capability of the capillary zone electrophoresis (CZE) operating buffer system to separate and quantify monoclonal antibodies by the CZE method. Triethylenetetramine can be used for the amination of polyacrylonitrile fibers to form new fiber catalysts for Knoevenagel condensation in aqueous media. TETA also acts as a copper(II) selective chelator. Triethylenetetramine (TETA) can also be used as a growth promoter in the formation of 1D zinc sulfide nanoarchitectures.

Triethylenetetramine (TETA) is a highly selective divalent Cu(II) chelator and orphan drug that reverses copper overload in tissues. The salt form of trientine (triethylenetetramine dihydrochloride or 2,2,2-tetramine) was introduced in 1969 as an alternative to D-penicillamine. It consists of a polyamine-like structure that differs from D-penicillamine in that it does not contain sulfhydryl groups. It was previously approved by the FDA in 1985 as second-line pharmacotherapy for Wilson's disease. Although penicillamine therapy is believed to be more comprehensive, Triethylenetetramine (TETA) therapy has been shown to be an effective initial therapy even in patients with initially decompensated liver disease, and long-term Triethylenetetramine (TETA) therapy is not associated with adverse effects. expected in penicillamine therapy. Its clinical applications in cancer, diabetes mellitus, Alzheimer's disease and vascular dementia are examined.

Triethylenetetramine (TETA) is an oral copper chelating agent used to treat Wilson's disease. Triethylenetetramine (TETA) has not been associated with worsening of serum enzyme elevations or cases of clinically evident liver injury with jaundice during treatment.

Triethylenetetramine appears as a yellowish liquid. Less dense than water. It is flammable, but can be difficult to ignite. It is corrosive to metals and tissues. Vapors are heavier than air. Toxic nitrogen oxides formed during combustion. It is used in detergents and in the synthesis of dyes, drugs and other chemicals.

Triethylenetetramine (TETA) is a copper chelator used as an alternative to D-penicillamine in the treatment of Wilson's disease. It tends to be used in patients who experience serious side effects due to penicillamine therapy or penicillamine intolerance.

Triethylenetetramine (TETA) is a selective copper (II) chelator. While neutralizing its catalytic activity, it binds tightly to the urine and facilitates the systemic elimination of Cu(II), but does not cause systemic copper deficiency even after long-term use. It can also act as an antioxidant, as it suppresses copper-mediated oxidative stress. Triethylenetetramine (TETA) not only increases urinary Cu excretion, but also reduces intestinal copper absorption by 80%.

The unchanged drug and two acetylated metabolites, N1-acetyltriethylenetetramine (MAT) and N1,N10-diacetyltriethylenetetramine (DAT), are excreted mainly in the urine. About 1% of the administered trientine and about 8% of the biotransformed trientine metabolite acetyltriene is ultimately seen in the urine. In parallel with the amount of trientine excreted in the urine, the amounts of copper, zinc and iron in the urine also increase. The unchanged drug after oral administration is also excreted in the feces.

Triethylenetetramine (TETA) is mainly metabolized by acetylation and two major acetylated metabolites are found in human serum and urine. Triethylenetetramine is readily acetylated as N1-acetyltriethylenetetramine (MAT) and N1,N10-diacetyltriethylenetetramine (DAT). MAT can still bind the divalent Cu, Fe and Zn, but to a much lesser extent compared to the unchanged drug. To date, no enzyme has been definitively identified as responsible for Triethylenetetramine acetylation, but spermidine/sperm acetyltransferase-1 (SSAT-1) is a potential candidate responsible for Triethylenetetramine acetylation due to the close chemical similarity between the natural substrate spermidine and Triethylenetetramine. . Triethylenetetramine (TETA) has also been shown to be an in vitro substrate for human thialysis acetyltransferase (SSAT2).

The plasma elimination half-life of triethylenetetramine in healthy volunteers and patients with Wilson's disease ranges from 1.3 to 4 hours. Metabolites are expected to be longer than the parent drug.

Because copper exhibits enhanced ligand binding properties for nitrogen compared to oxygen, the four components in a planar ring are chelated forming a stable complex with nitrogen. Cu(II) very tight

Thus, the bonds have a dissociation constant of 15 mol/L from Cu(II) at pH 7.0. Triethylenetetramine reacts with copper at a stoichiometric ratio of 1:1 and also in vivo with iron ande can form complexes with zinc. Triethylenetetramine (TETA) is considered a potential chemotherapeutic agent as it is a ligand for the G-quadruplex and can be a telomerase inhibitor as it stabilizes both intramolecular and intermolecular G-quadruplexes. May mediate a selective inhibitory effect on tumor growth or cytotoxicity. Chelation of excess copper can affect copper-induced angiogenesis. Other mechanisms of action of Triethylenetetramine (TETA) for alternative therapeutic applications include enhanced antioxidant defense against oxidative stress, pro-apoptosis and reduced inflammation.


Triethylenetetramine (TETA) A mixture of four compounds with close boiling points, including linear, branched and two cyclic molecules. Building block in the production of imidazoline-based corrosion inhibitors.

Triethylenetetramine Usage Areas:

corrosion inhibitors; wet strength resins;

Fabric softeners; Epoxy curing agents; polyamide resins; fuel additives; Lubricating oil additives; asphalt additives; ore flotation; corrosion inhibitors; Asphalt; Additives; Epoxy curing agents; Hydrocarbon purification; Mineral oil and fuel additives; mineral processing aids; polyamide resins; surfactants; Textile additives - paper wet strength resins; Fabric softeners; surfactants; Coatings; urethanes; fuel additives; Chemical intermediates; Epoxy curing agents; Mineral oils; Wet strength resins.

Benefits of Triethylenetetramine:

Consistent and predictable reaction products; It is easily derived; low vapor pressure; High viscosity; Low environmental impact; Suitable for harsh conditions; low sensitivity; Multidirectional.

Triethylenetetramine (TETA) / Ethanol Solutions

Zheng et al. They reported that triethylenetetramine (TETA) dissolved in ethanol can form a solid precipitate that can be easily separated and regenerated after CO2 absorption.19 In contrast, a Triethylenetetramine/water solution does not form any precipitate after CO2 absorption. The triethylenetetramine/ethanol solution offers several advantages for CO2 capture in terms of absorption rate, absorption capacity and absorbent regenerability. Both the rate and capacity of CO2 absorption with the triethylenetetramine/ethanol solution is significantly higher than that of the Triethylenetetramine/water solution. This is because ethanol not only increases the solubility of CO2 in the liquid phase, but can also facilitate the chemical reaction between Triethylenetetramine and CO2. It has been found that this approach can capture 81.8% of the CO2 absorbed in the solid phase as Triethylenetetramine-carbamate. Absorption-desorption tests using temperature fluctuation process reveal that the absorption performance of Triethylenetetramine/ethanol solution is relatively stable. A limitation of the use of Triethylenetetramine/ethanol solution for CO2 removal is that ethanol is a solvent with a high vapor pressure and measures must be taken to reduce solvent evaporation.

Small Organic Molecule Depressants

The polyamines DETA (diethylenetriamine) and TETA (triethylenetetramine), identified as a subgroup by Nagaraj and Ravishankar (2007), are used only in the processing of Ni ores to suppress pyrrhotite (Marticorena et al., 1994; Kelebek and Tukel, 1999). Although the mechanism is not fully understood, the N-C-C-N structure of amines is accidentally chelated with metal ions such as Cu and Ni, which can activate pyrrhotite. Precipitation of pyroxene (a silicate) by DETA and triethylenetetramine (TETA) in the selective flotation of pentlandite was attributed to this deactivation mechanism. In combination with sulfur ions to reduce potency, and hence reaction with xanthate (even dissociating into carbon disulfide) increases the effectiveness of polyamine suppressors.

Condensation of a poly (amine) such as diethylene triamine, triethylenetetramine or amino ethylethanolamine with C21 or C22 carbon fatty acids or tallow acids can be used as the corrosion inhibitory base. Propargyl alcohol has been found to enhance the anticorrosive effects of the composition.

Diethylenetriamine and triethylenetetramine are highly reactive primary aliphatic amines with five and six active hydrogen atoms for crosslinking, respectively. Both materials will cure glycidyl ether at room temperature. In the case of diethylenetriamine, the exothermic temperature can reach up to 250°C in batches of 200 g. With this amine, 9-10 pts phr, stoichiometric quantity is required and will give pot life less than one hour at room temperature. Actual time depends on ambient temperature and batch size. 12-13 points phr is required with triethylenetetramine. Both materials are used in small castings due to their high reactivity.

and laminates have the disadvantage of high volatility, sharpness and skin.

sensitivity. Properties such as heat distortion temperature (HDT) and volume resistivity are critically dependent on the amount of hardener used.


be a selective chelator of CuIIn triethylenetetramine (TETA) is widely used in the treatment of Wilson's disease. Recently, it has been shown that triethylenetetramine can be used in cancer treatment due to its telomerase inhibitor and anti-angiogenesis properties. Although triethylenetetramine has been used in the treatment of Wilson's disease for decades, a comprehensive review of the pharmacology of triethylenetetramine is not available. Triethylenetetramine is poorly absorbed and has a bioavailability of 8% to 30%. It is widely distributed in tissues with relatively high concentrations measured in the liver, heart and kidney. It is mainly metabolized by acetylation and two major acetylated metabolites are found in human serum and urine. It is excreted in the urine mainly as unchanged parent drug and two acetylated metabolites. It has a relatively short half-life (2 to 4 hours) in humans. Recent discoveries in triethylenetetramine (TETA) pharmacology show that the main pharmacokinetic parameters are not related to the acetylation phenotype of the traditionally accepted drug acetylation enzyme N-acetyltransferase 2, and that the enzyme that metabolizes Triethylenetetramine is actually spermidine/spermtransyltransin acetyltransin. This review also covers the current preclinical and clinical application of Triethylenetetramine. It provides a much-needed overview and updated information on triethylenetetramine pharmacology for clinicians or cancer researchers wishing to embark on cancer clinical trials using triethylenetetramine or its close structural analogues.

Triethylenetetramine (TETA), a selective chelator of CuII and an orphan drug, is widely used in the treatment of Wilson's disease. Recently, their potential use in cancer chemotherapy and other diseases has been investigated.

Wilson's disease is an autosomal recessive genetic disease characterized by copper accumulation in the tissues of patients. The disease, which manifested as neurological or psychiatric symptoms and liver disease, caused the death of patients and was considered an incurable disease until the 1950s. Treatment of this disease with orphan drugs was developed by John Walshe in the 1950s. Currently, common treatments for Wilson's disease either reduce copper absorption using zinc acetate or remove excess copper from the body using chelators such as penicillamine and Triethylenetetramine.

Recently, it has been shown that Triethylenetetramine can improve left ventricular hypertrophy in humans and rats with diabetes. Based on preclinical studies, it has also been suggested that Triethylenetetramine can be used in cancer treatment because it is a telomerase inhibitor and has anti-angiogenesis properties. In addition, a recent report showed that Triethylenetetramine treatment can overcome cisplatin resistance in human ovarian cancer cell culture through inhibition of superoxide dismutase 1/Cu/Zn superoxide dismutase. Another recent report showed that Triethylenetetramine can induce apoptosis in murine fibrosarcoma cells through activation of the p38 mitogen-activated protein kinase (MAPK) pathway. However, no clinical studies or trial plans using Triethylenetetramine to treat cancer have been reported in the literature. Since triethylenetetramine is an orphan drug and has been used in the clinic for decades, it can be easily tested in clinical cancer chemotherapy. However, a thorough understanding of Triethylenetetramine pharmacology is essential to reap the potential benefits of Triethylenetetramine in clinical cancer therapy.

Although triethylenetetramine (TETA) has been used in the treatment of Wilson's disease for decades, relatively few reports of Triethylenetetramine pharmacology in patients with Wilson's disease can be found in the literature, and to date there is no comprehensive review of Triethylenetetramine pharmacology. This overview examines the pharmacological aspects and current clinical applications of Triethylenetetramine (TETA), providing valuable information to research scientists or clinicians interested in using Triethylenetetramine as a treatment for cancer or other diseases. It also reveals gaps in Triethylenetetramine pharmacology that need to be addressed despite decades of clinical use in patients with Wilson's disease.

Chemistry and Detection

Triethylenetetramine (TETA) is a structural analogue of the linear polyamine compounds spermidine and spermine. It was first made in Berlin, Germany, in 1861, and was made as the dihydrochloride salt in 1896. Chelation activity was discovered at Cambridge University in 1925.

revised version. CuII prefers nitrogen to oxygen as a ligand, and Triethylenetetramine is suitable because it has four nitrogen groups. Square planar geometry where CuII is most stable. Therefore, CuII is very tightly bound, with a dissociation constant of 10−15 mol/.s.

L at pH 7.0.

Triethylenetetramine is clinically used mainly as its dihydrochloride salt (trientine; ref. 1, 16); however, a form of Triethylenetetramine disuccinate has also recently been developed. Trientine is soluble in aqueous solutions and is presented as a free-base Triethylenetetramine. Triethylenetetramine has proven difficult to detect in aqueous solutions because it has a very polar nature, does not separate efficiently from conventional high performance liquid chromatography (HPLC) columns, and has little absorption at accessible UV detection wavelengths. One solution inspired by aqueous polyamine analytical methods is to use fluorescent labeling reagents to derive Triethylenetetramine and detect its derivatives using a fluorimetric detector. A number of fluorescent labeling reagents have been tried, including m-toluoyl chloride, fluoresamine, dansyl chloride, O-phthalaldhit, 4-(1-pyrene)butyric acid N-hydroxysuccinimide ester, and 9-fluorenylmethylchloroformate. However, fluorimetric methods are associated with difficulties, such as whether the analyte is fully or partially labeled and whether the detected peaks are separated from other known or unknown metabolites, polyamines and their metabolites. Only one of the above methods resolved these concerns. An HPLC-conductivity detection method has also been developed, but the detection limit is relatively high, resulting in poor sensitivity to the method. Recently, a non-derivative method using liquid chromatography-mass spectrometry (LC-MS) has been developed to simultaneously detect Triethylenetetramine and its two major metabolites in aqueous solutions, providing more sensitive detection and analytical power. With the availability of LC-MS-MS technology, a method with higher sensitivity and accuracy can be developed to study Triethylenetetramine and its metabolites in human samples; this will certainly facilitate future pharmacological studies on Triethylenetetramine.


Mechanism of action in Wilson's disease

Triethylenetetramine (TETA) is a selective chelator for CuII that helps to systemically eliminate divalent Cu from the human body by forming a stable complex that is easily excreted by the kidney. Triethylenetetramine not only increases urinary Cu excretion, but also reduces intestinal copper absorption by 80%. Triethylenetetramine and its metabolite MAT can bind divalent Cu, Fe and Zn. However, the chelating activity of MAT is significantly lower than that of Triethylenetetramine. In healthy volunteers, urinary copper levels increase in parallel with the amount of Triethylenetetramine (TETA) excretion, while in diabetic patients it increases in parallel with the sum of Triethylenetetramine and MAT. Removal of excess Cu in Wilson's patients is considered the mechanism of action to treat this disease.


Triethylenetetramine can also be used to overcome cisplatin resistance in ovarian cancer cells by reducing overexpressed Cu/Zn superoxide dismutase. Combination therapy using cisplatin and triethylenetetramine may be a possible clinical entry point for Triethylenetetramine chemotherapy in cancer, as it is well understood that triethylenetetramine can reduce Cu/Zn superoxide dismutase overexpressed in human diseases.

Triethylenetetramine (TETA) Currently, there is no systemic study investigating the anticancer mechanisms of triethylenetetramine. To better understand the anticancer effects of triethylenetetramine, more systematically designed studies are needed to demonstrate the hierarchy of Triethylenetetramine action in cancer cells, and these will certainly guide or benefit future clinical practice.

Mechanism of action in other clinical applications

Recently, triethylenetetramine has been used in clinical trials for the treatment of diabetic heart failure. Copper homeostasis has been shown to be a pathogenic abnormality associated with hyperglycemia in type 2 diabetic patients. Triethylenetetramine treatment reduces left ventricular hypertrophy in patients. It also improves left ventricular function, repairs damaged aortic and left ventricular structures, and improves cardiac antioxidant defense in rat diabetes models. However, the precise targets and mechanism of action of triethylenetetramine in diabetic heart failure are still under investigation.

Triethylenetetramine is effective in the treatment of diabetic heart failure as well as other diabetic complications. One report demonstrated that Triethylenetetramine was effective in diabetic nephropathy by normalizing kidney fibrosis and through activation of pathogenic transforming growth factor-(TGF-) in a rat model.

is work. Two other reports produced data showing that Triethylenetetramine suppressed carbonyl stress and reduced inflammation in the lenses of diabetic rats. Therefore, triethylenetetramine can be used to help treat diabetic retinopathy. knows.

Current Clinical Practices and Therapeutic Effects

Triethylenetetramine (TETA) is currently used as second-line therapy in the form of trientine for W. for patients with ilson's disease, especially penicillamine allergy or intolerance. It is mostly used in children with Wilson's disease. The common dosing schedule is 600 mg/day twice daily and is mainly determined by plasma T1/2. Triethylenetetramine is also used in other metal poisonings. For example, one case reported that triantine was effective in treating manganese poisoning in a patient with acquired hepatocerebral degeneration.

Another clinical use of triethylenetetramine (TETA) is in diabetic complications. Triethylenetetramine has been used in clinical trials to treat diabetic heart failure and has been shown to be effective in patients diagnosed with type 2 diabetes with cardiac complications. Several preclinical animal studies have been conducted using Triethylenetetramine to treat diabetic nephropathy and retinopathy, and the results show that Triethylenetetramine is effective in improving these complications in diabetic animal models.

A number of preclinical in vivo and in vitro studies have been performed for the treatment of cancer using triethylenetetramine. However, only one clinical application of Triethylenetetramine in cancer has been reported. In this report, Triethylenetetramine was used to reduce liver copper content in patients with hepatocellular carcinoma (HCC) after percutaneous ethanol injection or radiofrequency ablation. showed that triethylenetetramine can reduce the copper content in liver tissue; this may be useful in the treatment of HCC because increased copper levels have been identified in association with the development of HCC.

In preclinical studies, Triethylenetetramine (TETA) has been shown to effectively inhibit the growth of various tumors or tumor cells, including neuroblastoma, HCC, HeLa cells, colorectal carcinoma, breast cancer cells (MCF-7), fibrosarcoma, and glioma. mechanisms of anti-angiogenesis, telomerase inhibition and apoptosis. In another study, Triethylenetetramine (TETA) exhibited the ability to overcome cisplatin resistance in human ovarian cancer cells through inhibition of Cu/Zn superoxide dismutase activity. Based on the same mechanism, Triethylenetetramine has been shown to be effective in the treatment of familial amyotrophic lateral sclerosis, a copper-mediated oxidative toxicity in a mouse model. According to an in vitro study, it has been suggested that Triethylenetetramine may be effective in the treatment of Alzheimer's disease.

Copper appears to be an essential element for angiogenesis in cancer cells. Tetrathiomolibate, a potent copper chelator, is currently in clinical trials for cancer. On the other hand, polyamine appears to play an important role in cancer nutrition, and a number of polyamine analogs are in clinical trials. As a copper-specific chelator and polyamine analogue with a relatively safe clinical profile and a different metabolic pathway from common cancer drugs, Triethylenetetramine is a good candidate for cancer chemotherapy or combination therapy.


Triethylenetetramine (TETA) is an established orphan drug with promising new clinical applications and results. Triethylenetetramine could be a promising anticancer agent with the potential to enter clinical trials very soon. It is also likely to be used in conjunction with cancer chemotherapy. Consequently, knowledge of its pharmacology is largely required. This review provides an overview of the known pharmacology of Triethylenetetramine based on the available information. Although triethylenetetramine (TETA) has been used in clinical situations for decades, information on its pharmacology is still limited. For example, many pharmacological aspects of triethylenetetramine have not been fully elucidated, such as the exact mechanism of absorption in humans, the effect of co-administration on zinc absorption, which food components inhibit absorption, how it is released from cells and how it passes. researched. the blood-brain barrier, its effect on excretion of renal failure, and its full-range mechanism of action in cancer therapy. Recent research on its metabolism suggests that it may be an ideal candidate for combination chemotherapy, as it is metabolized by a unique SSAT pathway that is unlikely to interfere and/or interfere with the metabolism of normal anticancer drugs. More pharmacological information about Triethylenetetramine is still needed, especially in population groups with diseases such as cancer and diabetes patients. A thorough understanding of the pharmacology of triethylenetetramine necessary for its therapeutic adoption.






Trientine (INN)




Syprine (brand name)


EPH 925









triethylene tetramine

Araldite hardener HY 951


Araldite HY 951






Trientinum [INN-Latin]

NSC 443

Trientina [INN-Spanish]



CCRIS 6279

Ethylenediamine, N,N'-bis(2-aminoethyl)-

HSDB 1002


EINECS 203-950-6




1,2-Ethanediamine, N1,N2-bis(2-aminoethyl)-


Triethylenetetramine, 60%


trientine; trientina






EPH 925

Trientine [INN]


tomography, x-ray computed trientine

triethylene tetraamine



Texlin 300 (Salt/Mixture)


Triethylenetetramine, >=97.0% (T)

Ethylenediamine, N'-bis(2-aminoethyl)-

Ethanediamine, N,N'-bis(2-aminoethyl)-


Triethylenetetramine [UN2259] [Corrosive]

Triethylenetetramine, technical grade, 60%

Triethylenetetramine [UN2259] [Corrosive]



1,2-Ethanediamine, N1,N2-bis(2-aminoethyl)- [ACD/Directory Name]


112-24-3 [RN]


N,N'-Bis(2-aminoethyl)-1,2-ethanediamine [German] [ACD/IUPAC Name]

N,N'-Bis(2-aminoethyl)-1,2-ethanediamine [ACD/IUPAC Name]

N,N'-Bis(2-aminoethyl)-1,2-ethanediamine [French] [ACD/IUPAC Name]



trientina [Spanish] [INN]

trientine [French] [INN]

trientinum [Latin] [INN]

triethylene tetramine




1,2-Ethanediamine, N,N'-bis(2-aminoethyl)-

1,2-Ethanediamine, N1,N2-bis(2-aminoethyl)-



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