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US Previously Marketed

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Primary Target

Taste receptor type 1 member 2

5

Taste receptor type 1 member 3

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Approval Year

1921

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Unknown

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Originator

Remsen, I.|Fahlberg, C.

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Chemical

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CAS

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EPA CompTox

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PUBCHEM

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DAILYMED

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Salts, Hydrates, Esters, etc.

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Showing 1 - 6 of 6 results

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METHYLTHIADIAZOLE THIOL

9JY8UF0TSS

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Status:

Other

Class (Stereo):

CHEMICAL (ACHIRAL)

SACCHARIN

FST467XS7D

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Status:

US Previously Marketed

First marketed in 1921

Class (Stereo):

CHEMICAL (ACHIRAL)

Targets:

Taste receptor type 1 member 3

Taste receptor type 1 member 2

Conditions:

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

SACCHARIN SODIUM MONOHYDRATE

A9CO00M9HV

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Status:

US Previously Marketed

First marketed in 1921

Class (Stereo):

CHEMICAL (ACHIRAL)

Targets:

Taste receptor type 1 member 3

Taste receptor type 1 member 2

Conditions:

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

SACCHARIN SODIUM

SB8ZUX40TY

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Status:

US Previously Marketed

First marketed in 1921

Class (Stereo):

CHEMICAL (ACHIRAL)

Targets:

Taste receptor type 1 member 3

Taste receptor type 1 member 2

Conditions:

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

AMMONIUM SACCHARIN

63Q3BCF15A

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Status:

US Previously Marketed

First marketed in 1921

Class (Stereo):

CHEMICAL (ACHIRAL)

Targets:

Taste receptor type 1 member 3

Taste receptor type 1 member 2

Conditions:

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

SACCHARIN SODIUM ANHYDROUS

I4807BK602

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Status:

US Previously Marketed

First marketed in 1921

Class (Stereo):

CHEMICAL (ACHIRAL)

Targets:

Taste receptor type 1 member 3

Taste receptor type 1 member 2

Conditions:

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

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