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Details

Stereochemistry ACHIRAL
Molecular Formula C7H4NO3S.H4N
Molecular Weight 200.215
Optical Activity NONE
Defined Stereocenters 0 / 0
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of AMMONIUM SACCHARIN

SMILES

[NH4+].O=C1[N-]S(=O)(=O)C2=C1C=CC=C2

InChI

InChIKey=XTPLQANXHDDXIH-UHFFFAOYSA-N
InChI=1S/C7H5NO3S.H3N/c9-7-5-3-1-2-4-6(5)12(10,11)8-7;/h1-4H,(H,8,9);1H3

HIDE SMILES / InChI

Description

Saccharin is the most established of the artificial sweeteners on the market, this mixture of dextrose and saccharin has been in use for over a century and is found in diet versions of soft drinks. It is 300-500 times sweeter than sugar and contains zero calories. In 1977, the FDA tried to ban its use after evidence showed it caused cancer in rats. Extensive lobbying by the diet food industry allowed products to stay on the shelves as long as they carried warnings about the cancer risks in animals. This warning was removed in 2001 when the Calorie Control Council insisted the link between animal and human cancers could not automatically be made. Consumption of saccharin-sweetened products can benefit diabetics as the substance goes directly through the human digestive system without being digested. While saccharin has no food energy, it can trigger the release of insulin in humans due to its sweet taste. The T1R2/R3 sweet taste receptor exist on the surface of pancreatic beta cells. Saccharin is a unique in that it inhibits glucose-stimulated insulin secretion (GSIS) at submaximal and maximal glucose concentrations, with the other sweeteners having no effect. Investigation of saccharin’s dose-response characteristics showed that concentrations of 0.1 and 0.5 mM stimulated insulin secretion, while concentrations of 1 and 2.5 mM inhibited insulin secretion. Saccharin’s effect on insulin secretion was shown to be reversible in INS-1 832/13 clonal pancreatic beta cells after chronic exposure to 1 mM saccharin. Artificial sweeteners may affect insulin secretion via interaction with the sweet taste receptor, also saccharin may affect other cellular processes linked to insulin secretion, and that these effects are both time- and concentration-dependent

Originator

Approval Year

Targets

Primary TargetPharmacologyConditionPotency

Conditions

ConditionModalityTargetsHighest PhaseProduct

Cmax

ValueDoseCo-administeredAnalytePopulation
14 μg/mL
2 g single, oral
SACCHARIN plasma
Homo sapiens
27 μg/mL
2 g single, oral
SACCHARIN plasma
Homo sapiens

AUC

ValueDoseCo-administeredAnalytePopulation
5800 μg × min/mL
10 mg/kg single, intravenous
SACCHARIN plasma
Homo sapiens
3700 μg × min/mL
10 mg/kg single, intravenous
SACCHARIN plasma
Homo sapiens
6500 μg × min/mL
2 g single, oral
SACCHARIN plasma
Homo sapiens
6800 μg × min/mL
2 g single, oral
SACCHARIN plasma
Homo sapiens

Overview

CYP3A4CYP2C9CYP2D6hERG

OverviewOther

Other InhibitorOther SubstrateOther Inducer



Drug as perpetrator​

Drug as victim

PubMed

Sample Use Guides

In Vivo Use Guide
no more than 80 to 3000 mg saccharin per kilogram or litre should be used
Route of Administration: Oral
In Vitro Use Guide
After assaying for prolactin (PRL) in saccharin-treated cultures, it was observed that this sweetener is also capable of stimulating PRL production two- to sixfold in a dose-dependent manner. Enhancement of PRL production can be observed at 0.5 mM saccharin, yet this is 10 times less than the saccharin concentration required to alter cell shape. These effects of saccharin on cell morphology and on PRL production are reversible in rat pituitary tumor cells (GH4C1). When added to cultures along with maximal concentrations of epidermal growth factor (EGF) or thyrotropin-releasing hormone (TRH), the effects of saccharin on PRL production are additive, suggesting that the actions of saccharin are mediated by a somewhat different pathway from that of the peptide hormones