Aspartame is made up of methanol, aspartate, an excitatory neurotransmitter in the central nervous system, and phenylalanine, which is vital for neurotransmitter modulation [2].

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Aspartame (4000 mg/kg bw/day; oral) did not cause any negative effects in mice, rats, hamsters, or dogs in acute, subacute, or long-term toxicity investigations of aspartame and its breakdown products[1].

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In infant mice (8-day-old Swiss-Webster strain), oral administration of Aspartame at doses equivalent to 500 mg/kg body weight was the highest dose that did not result in neuronal necrosis; doses of 750 or 1000 mg/kg induced neuronal necrosis [1].

In male CD-1 mice, oral bolus doses of Aspartame at 1000 mg/kg or higher increased the percentage of animals convulsing in response to pentylenetetrazole or fluorothyl; the CD50 for mice treated with both pentylenetetrazole and 1 g/kg aspartame was reduced to 59 mg/kg compared to 66 mg/kg for pentylenetetrazole alone [1].

In male Sprague-Dawley rats, oral gavage of Aspartame at 1000 mg/kg (bolus dose to fasted rats) lowered the ED50 of metrazol-induced convulsions from 65.9 mg/kg to 50.7 mg/kg; no effect was observed when the same dose was divided into three doses over 120 min or given to non-fasted rats [1].

In male Sprague-Dawley rats, a single oral dose of Aspartame at 200 mg/kg increased brain levels of phenylalanine (116±4 nmol/g vs. 94±8 in controls), tyrosine (224±7 vs. 169±8), but did not affect tryptophan (14±1 vs. 19±1); no differences in brain monoamine transmitter concentrations (serotonin, 5-HIAA, dopamine, norepinephrine, DOPAC, HVA) were observed [1].

In rats fed Aspartame at 500 mg/kg/day for 30 days, no changes in plasma or brain levels of tyrosine, phenylalanine, alanine, valine, methionine, aspartic acid, or glutamic acid were found [1].

In a 13-week double-blind study in healthy children (2–21 years) consuming Aspartame at 27–77 mg/kg bw/day, no differences in plasma amino acid levels, blood methanol, or adverse effects were observed between aspartame and sucrose groups [1].

In a 24-week double-blind placebo-controlled study in 108 healthy adults consuming Aspartame at 75 mg/kg bw/day, no significant changes in body weight, vital signs, blood lipids, plasma amino acids (except a transient increase in tyrosine within normal range), blood methanol (mostly below detection limit of 0.31 mmol/L), or adverse effects were observed [1].

In a prospective epidemiological study (n=473,984) with up to 5 years follow-up, no significant associations were found between Aspartame consumption and risk of hematopoietic cancers (adjusted RR for ≥600 mg/day vs. none = 0.98, 95% CI 0.76–1.27) or gliomas (RR for ≥400 mg/day vs. none = 0.73, 95% CI 0.46–1.15) [1].

In animal studies, Aspartame administered orally at doses up to 4000 mg/kg/day in chronic studies showed no adverse effects [1]. [1]

In mice, a single oral dose of Aspartame increased norepinephrine and dopamine concentrations in various brain regions; repeated dosing decreased serotonin and its metabolite 5-hydroxyindoleacetate in several regions [2].

Human and pig intestinal microvillar membrane preparations were incubated with Aspartame (1 mM) and specific peptidase inhibitors (0.1 mM) to identify the primary peptidase responsible for hydrolysis. Aspartame and α-aspartylphenylalanine were rapidly metabolized, while β-aspartame and DKP were not. Inhibition of aminopeptidase A showed the greatest impact on aspartame metabolism, indicating this as the major peptidase [1].

In vitro incubation of rat pancreatic islets with Aspartame at concentrations of 1.0 to 10 mM failed to induce increased insulin release, regardless of the presence or absence of D-glucose [1].

In a study with rats fed Aspartame at 40 or 4000 mg/kg/day for 45 or 90 days, liver microsomal enzyme activities (7-ethoxycoumarin deethylase, epoxide hydrolase, carboxylesterase, p-nitrophenol UDP-glucuronosyltransferase, glutathione S-transferases, and cytochrome P-450 content) were evaluated. At 45 days, epoxide hydrolase, carboxylesterase, and UDP-glucuronosyltransferase were elevated in the high-dose group, but these differences were no longer present after 90 days [1].

Human erythrocyte membranes were incubated for 1 hour with combinations of methanol, aspartic acid, and phenylalanine at concentrations estimated to represent blood levels following aspartame doses of 10–200 mg/kg bw. Acetylcholinesterase activity was inhibited in a dose-dependent manner. The five combinations of metabolites (from lowest to highest corresponding doses) inhibited erythrocyte acetylcholinesterase activity by 0%, 7%, 33%, 41%, and 57%, respectively. However, the relevance of these findings is questionable as blood methanol levels are below detection limits in humans consuming 34 mg/kg bw aspartame [1].

In vitro hippocampal slice preparation was used to evaluate Aspartame as a neuroexcitatory agent. Exposure of hippocampal slices to aspartame at 0.01, 0.1, 1, and 10 mM potentiated the response of CA1 pyramidal cells but had no effect on local inhibitory systems or on long-term potentiation induction [1].

Mouse NB2a neuroblastoma cells were grown in culture, and differentiation was induced by dibutyryl cyclic AMP and serum removal, leading to neurite outgrowth. Addition of Aspartame to the culture media was reported to inhibit neurite growth. However, because aspartame is completely hydrolyzed in the gut and not detected in plasma following oral administration, this finding is not considered relevant to human exposure [1].

The estrogenic activity of Aspartame was examined using the estrogen receptor-dependent breast cancer cell line MCF-7 at concentrations up to 1000 μg/ml; no evidence of estrogenic activity was observed [1].

Primary rat hepatocyte cultures derived from Sprague-Dawley rats were incubated with 5 or 10 mM Aspartame for 20 hours to assess DNA repair; no evidence of DNA-damaging activity was found [1].

Acute oral toxicity studies: Aspartame was administered orally to mice, rats, and rabbits at doses up to 10,000 mg/kg body weight. No deaths or adverse effects were observed at the highest doses tested [1].

Subchronic oral toxicity studies: Mice received Aspartame in the diet at doses up to 13,000 mg/kg/day for 28 days; rats received up to 10,000 mg/kg/day for 63 days; dogs received up to 6,000 mg/kg/day for 8 weeks. No adverse effects were reported at the highest doses [1].

Chronic toxicity and carcinogenicity studies: Aspartame was administered in the diet to mice, rats, hamsters, and dogs at doses up to 4,000 mg/kg/day for up to 2 years. No adverse effects were consistently found [1].

Transgenic mouse carcinogenicity studies (p53+/-, Cdkn2a-deficient, and Tg.AC models): Aspartame was mixed in NTP 2000 feed at concentrations of 0, 3125, 6250, 12,500, 25,000, and 50,000 ppm (equivalent to up to 7,500 mg/kg/day), administered for 39 weeks. No neoplasms attributed to aspartame were observed in any dose group [1].

Neurotoxicity studies in rats: Aspartame was administered by gavage at various doses up to 2,000 mg/kg using different protocols (fasting, non-fasting, single bolus vs. divided doses). No consistent proconvulsant effect was observed at doses below 1,000 mg/kg. Some studies using bolus doses of 1,000 mg/kg or higher in fasted rats reported enhanced chemically-induced seizure incidence, but this was not a consistent finding [1].

Reproductive and developmental toxicity studies: Aspartame was administered orally to rats (up to 4,000 mg/kg/day), rabbits (up to 3,000 mg/kg/day), and hamsters during gestation and lactation. NOAELs for reproductive toxicity ranged from 1,600 mg/kg/day in rabbits to 4,000 mg/kg/day in rodents. Adverse effects on pup development occurred only at doses exceeding 5,000 mg/kg/day [1].

Human clinical study: 108 healthy adults consumed Aspartame at 75 mg/kg/day in capsules (three 300 mg capsules per day) for 24 weeks in a randomized, double-blind, placebo-controlled, parallel-group design. Extensive clinical laboratory measurements (body weight, vital signs, complete blood count, serum chemistry, plasma lipids, plasma amino acids, blood methanol, urinary formate, etc.) were conducted at baseline and at multiple time points. No significant differences were found between aspartame and placebo groups [1].

Absorption, Distribution and Excretion
Aspartame is absorbed in the small intestine, and its metabolism and absorption are very rapid. Metabolism/Metabolites Approximately 10% of aspartame (by weight) is broken down into methanol in the small intestine. Most of the methanol is absorbed and rapidly converted into formaldehyde. Approximately 50% of aspartame (by weight) is broken down into phenylalanine. Approximately 40% of aspartame (by mass) is broken down into aspartic acid. Unlike some other high-sugar sweeteners, aspartame is metabolized in the body and therefore has some nutritional value: 1 gram of aspartame provides approximately 17 kilojoules (4 kilocalories) of energy. However, in practice, small amounts of aspartame ingested produce almost no nutritional benefit. Aspartame's use has been a subject of considerable concern because it generates potentially toxic metabolites such as methanol, aspartic acid, and phenylalanine. Of these substances, only phenylalanine is produced in amounts sufficient to cause concern at normal aspartame intake levels. Aspartame [SC-18862; methyl 3-amino-N-(α-carboxyphenylethyl)succinate, methyl aspartate] is a sweetener with a sensory sweetness approximately 180 times that of sucrose. The metabolism of aspartame has been studied in mice, rats, rabbits, dogs, monkeys, and humans. Results show that aspartame is digested in the same manner as its natural dietary components in all species. Intestinal esterases hydrolyze the methyl group to methanol, which is then oxidized to carbon dioxide in a single-carbon metabolic pool. The resulting dipeptide is cleaved by dipeptidase on the mucosal surface, and the free amino acids are absorbed. The aspartic acid portion is primarily converted to carbon dioxide via the tricarboxylic acid cycle. Phenylalanine is mainly incorporated into proteins in vivo, primarily in its original form or as its major metabolite, tyrosine. Although aspartame is hydrolyzed in the monkey intestine to its components methanol, aspartic acid, and phenylalanine, continuous intake of 15 or 60 mg/kg doses of aspartame for 10 days did not alter the metabolism of phenylalanine. Aspartame has minimal effect on the disappearance of intravenously injected (14)C-phenylalanine from plasma, little effect on the conversion of phenylalanine to tyrosine or carbon dioxide, and does not alter the rate of label incorporation into proteins. Most of the phenylalanine derived from aspartame is incorporated into proteins in vivo, with only 20-25% of the compound being excreted. 60-80% of the derived methanol and aspartic acid are oxidized to carbon dioxide. For more complete metabolite/metabolite data on aspartame (7 metabolites), please visit the HSDB record page.
Biological Half-Life
At room temperature, aspartame is most stable at pH 4.3, with a half-life approaching 300 days. At pH 7, its half-life shortens to only a few days.

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Aspartame is completely hydrolyzed in the gastrointestinal tract by esterases and peptidases into three components: aspartic acid (40%), phenylalanine (50%), and methanol (10%). Aspartame does not enter the circulation prior to hydrolysis [1].

In humans, following oral administration of Aspartame at doses up to 200 mg/kg, no aspartame or aspartylphenylalanine is detectable in blood (detection limit 0.5 μmol/100 ml) [1].

Phenylalanine is absorbed into the portal blood and partially converted to tyrosine by hepatic phenylalanine hydroxylase. Aspartic acid is metabolized within enterocytes via transamination producing oxaloacetate, reducing the amount entering the portal circulation. Methanol is rapidly absorbed into portal blood and oxidized in the liver to formaldehyde (half-life 1–2 minutes), then to formic acid, and finally to CO2 and water [1].

In healthy adults given a single oral bolus dose of Aspartame at 34 mg/kg bw, blood methanol levels remained below the detection limit (0.4 mg/dl). At higher doses (100, 150, 200 mg/kg), blood methanol increased dose-dependently, peaking at 2.5 mg/dl at 2 hours after the 200 mg/kg dose. Blood formate levels did not change significantly, but urinary formate excretion increased [1].

In rats, the half-life of Aspartame in aqueous solution at pH 4–5, 25°C is over 250 days. Degradation products include DKP (diketopiperazine), α-aspartylphenylalanine, L-aspartic acid, L-phenylalanine, and L-phenylalanine methyl ester [1].

Effects During Pregnancy and Lactation
◉ Overview of Medication Use During Lactation
Aspartame is rapidly broken down in the mother's body and is therefore undetectable in breast milk. Ingesting very large amounts of aspartame (equivalent to 17 cans of soda or 100 packets of Equal sweetener) may slightly increase the phenylalanine content in breast milk. After a single large dose of aspartame, the phenylalanine concentration in breast milk returns to baseline levels within 12 hours. While as a precaution, aspartame should be avoided by breastfeeding women with infants with phenylketonuria (PKU), the amount usually ingested from aspartame-containing foods and beverages does not pose any additional risk to breastfed infants with PKU. Drinking sugar-free beverages containing low-calorie sweeteners may increase the risk of vomiting in breastfed infants. Studies have found an association between low-calorie sweeteners, particularly aspartame, and the risk of autism in boys, but more data are needed to establish a causal relationship.
◉ Effects on Breastfed Infants
A cross-sectional survey assessed the dietary history of US mothers between 11 and 15 weeks after their infants' birth. The survey was used to estimate the amount of sugar-free soft drinks and fruit juices consumed by these women. There were no statistically significant differences in infant weight or z-scores based on the intake of low-calorie sweeteners. However, infants who consumed low-calorie sweeteners in their milk once a week or less had a significantly higher risk of vomiting than infants who did not. Increased intake was not associated with vomiting. The effects of specific sweeteners could not be assessed.
A retrospective dietary recall study compared the relationship between consumption of sugar-free soft drinks and aspartame during pregnancy and/or lactation and the risk of autism in children. In boys, autism was associated with a three-fold increased likelihood of aspartame exposure. No statistically significant association was found in girls. The risk of exposure during breastfeeding was not separated from the risk of exposure during pregnancy, and whole aspartame is not typically found in breast milk; therefore, based on these data, it cannot be concluded that breastfeeding exposure causes autism. The authors suggest that methanol metabolites may have effects on infants.
◉ Effects on Lactation and Breast Milk
As of the revision date, no relevant published information was found.

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Interactions
...If mice are given a dose of aspartame sufficient to raise plasma phenylalanine levels above tyrosine levels..., the frequency of seizures increases after administration of the epileptogenic drug pentylenetetrazol. Equimolar amounts of phenylalanine can mimic this effect, while co-administration of valine (a substance that blocks phenylalanine from entering the brain) can block this effect. Aspartame can also enhance the effects of inhaled fluoxetine or electroconvulsive therapy on seizures...
This study investigated the antimutagenic effects of aspartame (0.4 and 4 mg/kg) in combination with β-carotene (0.15–15 mg/kg) by assessing chromosomal aberrations in bone marrow cells of C57Bl/6 mice. Single and continuous 5-day administration of the combination reduced the chromosome breakage effects of dioxane and cyclophosphamide and produced a more potent and broader antimutagenic effect than either component alone. This study aimed to investigate the analgesic and anti-inflammatory properties of the artificial sweetener aspartame, and its potential synergistic effects when used in combination with various opioids and nonsteroidal anti-inflammatory drugs (NSAIDs). Oral administration of aspartame (2–16 mg/kg) significantly increased the pain threshold in mice to acetic acid-induced writhing responses. Combination administration of aspartame (2 mg/kg, orally) with nimesulide (2 mg/kg, orally) and naproxen (5 mg/kg, orally) significantly reduced acetic acid-induced writhing responses compared to either drug alone. Similarly, combination administration of morphine (1 mg/kg, orally) or pentazocine (1 mg/kg, orally) with aspartame also reduced the frequency of writhing responses compared to aspartame or morphine alone, or pentazocine or a combination thereof. Combination administration of aspartame (4, 8, 16 mg/kg, orally) with nimesulide (2 mg/kg, orally) significantly reduced carrageenan-induced paw volume enlargement in rats and reversed nimesulide-induced hyperalgesia. Studies have shown that aspartame itself has analgesic and anti-inflammatory effects and exhibits synergistic analgesic effects with both opioid and non-opioid conventional analgesics. Ochratoxin A (OTA) is a fungal toxin produced by Asteris ochraceus and other molds. This fungal toxin contaminates animal feed and food. OTA has been shown to be immunosuppressive, genotoxic, teratogenic, carcinogenic, and nephrotoxic in all animal species studied to date. OTA inhibits protein synthesis and induces lipid peroxidation. Since it appears impossible to completely avoid food contamination by toxin-producing fungi, it is necessary to investigate possible methods to limit such toxicity. An in vivo study attempted to use aspartame (L-aspartyl-L-phenylalanine methyl ester) to prevent nephrotoxic and genotoxic effects of ochratoxin A (OTA), primarily affecting nuclear macrophages. Aspartame is a structural analog of OTA and phenylalanine. Aspartame (25 mg/kg body weight) prevents most of the nephrotoxic effects caused by OTA (289 μg/kg body weight). It also shows some effectiveness in preventing morphological and histological damage, primarily to nuclear macrophages. For more complete data on interactions of aspartame (9 items in total), please visit the HSDB record page.

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Acute oral LD50 of Aspartame in mice and rats is >10,000 mg/kg body weight; no adverse effects observed at the highest tested dose [1].

Subchronic NOAEL: mice >13,000 mg/kg/day; rats >10,000 mg/kg/day; dogs >6,000 mg/kg/day [1].

Chronic NOAEL: up to 4,000 mg/kg/day in rodents and dogs; no evidence of carcinogenicity in multiple long-term studies including transgenic mouse models (up to 7,500 mg/kg/day) [1].

Neurotoxicity: No consistent evidence of neuronal damage, seizure enhancement, or behavioral changes in animals or humans at doses relevant to human consumption. In infant monkeys given 2,000 mg/kg aspartame (or combined with 1,000 mg/kg MSG), no hypothalamic neuronal necrosis was observed despite elevated plasma phenylalanine and aspartic acid [1].

Reproductive/developmental toxicity: NOAELs of 1,600–4,000 mg/kg/day; no teratogenic effects [1].

Genotoxicity: Aspartame is nongenotoxic in Ames tests (up to 5,000 μg/plate), in vitro chromosomal aberration assays, in vivo micronucleus tests, and comet assays (2,000 mg/kg in mice) [1].

Human adverse effects: Double-blind placebo-controlled studies in self-reported sensitive individuals found no evidence of allergic reactions (urticaria/angioedema) or headaches attributable to aspartame. FDA passive surveillance (3,326 complaints as of 1988) did not establish a causal link between aspartame and any consistent symptom pattern [1].

Formaldehyde safety: The amount of formaldehyde generated from aspartame-derived methanol is trivial compared to endogenous production (>50,000 mg/day in an adult human) and dietary sources (e.g., one cup of coffee produces 30 mg formaldehyde from caffeine demethylation) [1].

[1]. Aspartame: a safety evaluation based on current use levels, regulations, and toxicological and epidemiological studies. Crit Rev Toxicol, 2007. 37(8): p. 629-727.

[2]. Humphries, P., E. Pretorius, and H. Naude, Direct and indirect cellular effects of aspartame on the brain. Eur J Clin Nutr, 2008. 62(4): p. 451-62.

Aspartame is a dipeptide formed by the condensation of the α-carboxyl group of L-aspartic acid and the amino group of L-phenylalanine methyl ester. It is commonly used as an artificial sweetener. Aspartame has multiple functions, including as a sweetener, nutritional supplement, micronutrient, exogenous substance, environmental pollutant, apoptosis inhibitor, and EC 3.1.3.1 (alkaline phosphatase) inhibitor. It is a dipeptide, carboxylic acid, and methyl ester. Its functions are related to L-aspartic acid and L-phenylalanine methyl ester. It is a zwitterionic tautomer of aspartame. A sweeter flavoring agent than sugar, metabolized to phenylalanine and aspartic acid.
A sweeter flavoring agent than sugar, metabolized to phenylalanine and aspartic acid.
Pharmaceutical indications
Used as a dietary supplement and sugar substitute.
Mechanism of action
180 to 200 times sweeter than sucrose, metabolized to protein, with subsequent amino acids consumed in their respective metabolic mechanisms.

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Therapeutic Uses
Aspartame is used as a potent sweetener…in pharmaceutical preparations, including tablets, powder mixtures, and vitamin formulations. It enhances flavor and can be used to mask certain unpleasant tastes; its sweetness is approximately 80-200 times that of sucrose.Drug Warnings
Aspartame is a methyl ester of a dipeptide composed of two amino acids, phenylalanine and aspartic acid. …Patients with phenylketonuria (PKU) must strictly limit their intake of phenylalanine; therefore, attention must be paid to the presence of phenylalanine in this medication and the amount of phenylalanine in each dose.
Patients with PKU should avoid excessive use of aspartame.
Aspartic acid and monosodium glutamate (MSG) are both neuroexcitatory amino acids, and they have additive toxicity to hypothalamic neurons. Because this can cause particularly significant harm to young children who have already ingested gram-level MSG in their diet, aspartame should generally not be added to children's foods.
Reported adverse reactions include headache; grand mal seizures; memory loss; gastrointestinal symptoms; and skin symptoms. However, scientifically controlled peer-reviewed studies have consistently failed to provide evidence of a causal relationship between aspartame intake and adverse health events… For more complete data on aspartame (8 total), please visit the HSDB records page.

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Pharmacodynamics
Aspartame (L-α-aspartic-L-phenylalanine methyl ester) is a low-calorie sweetener used to sweeten a variety of low-calorie and reduced-calorie foods and beverages, including low-calorie table sweeteners. Aspartame is composed of two amino acids: aspartic acid and phenylalanine, which exist in the form of methyl esters. Aspartic acid and phenylalanine are also naturally found in protein-containing foods, including meat, grains, and dairy products. Methyl esters are also naturally found in many foods, such as fruits, vegetables, and their juices. Aspartame is digested and broken down into three components (aspartic acid, phenylalanine, and methanol). These components are then absorbed into the bloodstream and participate in normal physiological processes. Neither aspartame nor its components accumulate in the body. These components are utilized in the same way as when obtained from ordinary food.

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Aspartame (N-L-α-aspartyl-L-phenylalanine 1-methyl ester) is a synthetic nonnutritive sweetener approximately 200 times sweeter than sucrose. It is used in over 90 countries in more than 6,000 products, including soft drinks, chewing gum, yogurts, puddings, tabletop sweeteners, and pharmaceuticals [1].

In the United States, the FDA established an Acceptable Daily Intake (ADI) of 50 mg/kg body weight/day; the European Food Safety Authority (EFSA) established an ADI of 40 mg/kg/day. Current consumption levels (mean 4.9 mg/kg/day, 95th percentile 13.3 mg/kg/day in the U.S.) are well below these ADIs [1].

Aspartame is stable in dry form but degrades in aqueous solutions at high temperatures and extreme pH. Degradation results in loss of sweetness and formation of DKP (diketopiperazine) and other breakdown products. DKP is naturally present in many foods (e.g., milk, dried shrimp, cheese, coffee, beer) at concentrations up to 6,576 pmol/g [1].

Aspartame is approved by the FDA and requires a label statement: "Phenylketonurics: contains phenylalanine" to warn individuals with phenylketonuria (PKU) who cannot metabolize phenylalanine [1].

Proposed mechanisms of neurotoxicity: Aspartame-derived phenylalanine competes with large neutral amino acids (including tryptophan and tyrosine) for transport across the blood-brain barrier via the large neutral amino acid transporter (NAAT). This competition may reduce brain synthesis of dopamine (from tyrosine) and serotonin (from tryptophan). Aspartame-derived aspartic acid may act as an excitatory neurotransmitter agonist on NMDA receptors. Methanol is metabolized to formaldehyde and formate, which can form adducts with proteins and nucleic acids [2].

Controversy remains regarding potential links to headaches, seizures, and behavioral disorders, but large-scale epidemiological and clinical studies have not confirmed causal associations [1][2].

C14H18N2O5

294.3

294.121

22839-47-0

Aspartame-d5;1356849-17-6;Aspartame acesulfame;106372-55-8;Aspartame-d3;1356841-28-5

134601

White to off-white solid powder

1.3±0.1 g/cm3

535.8±50.0 °C at 760 mmHg

242-248 °C

277.8±30.1 °C

0.0±1.5 mmHg at 25°C

1.557

1.11

3

6

8

21

380

2

COC(=O)[C@H](CC1=CC=CC=C1)NC(=O)[C@H](CC(=O)O)N

IAOZJIPTCAWIRG-QWRGUYRKSA-N

InChI=1S/C14H18N2O5/c1-21-14(20)11(7-9-5-3-2-4-6-9)16-13(19)10(15)8-12(17)18/h2-6,10-11H,7-8,15H2,1H3,(H,16,19)(H,17,18)/t10-,11-/m0/s1

(3S)-3-Amino-4-[[(2S)-1-methoxy-1-oxo-3-phenylpropan-2-yl]amino]-4-oxobutanoic acid

Nutrasweet Asp-phe-ome AspartamAsp-Phe methyl ester

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

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

DMSO : ~25 mg/mL (~84.95 mM)
H2O : ~5 mg/mL (~16.99 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (8.49 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (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 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (8.49 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (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 25.0 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 3: ≥ 2.5 mg/mL (8.49 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 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: 18.33 mg/mL (62.28 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

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