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US Approved Rx

38

US Previously Marketed

2

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Primary Target

3'(2'),5'-bisphosphate nucleotidase 1

30

Glycogen synthase kinase-3 beta

30

neurotrophin signaling pathway

30

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Highest Phase

Approved

40

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Approval Year

1921

40

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Condition

Bipolar disorder, manic episodes

30

Bowel Cleanser

8

Surgical Blood Losses

2

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Treatment Modality

Primary

32

Palliative

8

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CNS Activity

CNS Active

30

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Originator

Arfvedson, J.A.

30

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Chemical

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CAS

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FDA UNII

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PUBCHEM

40

EPA CompTox

38

ECHA (EC/EINECS)

26

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ATC Level 1

NERVOUS SYSTEM

2

ALIMENTARY TRACT AND METABOLISM

1

BLOOD AND BLOOD FORMING ORGANS

1

DERMATOLOGICALS

1

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ATC Level 2

PSYCHOLEPTICS

2

BLOOD SUBSTITUTES AND PERFUSION SOLUTIONS

1

DIGESTIVES, INCL. ENZYMES

1

OTHER DERMATOLOGICAL PREPARATIONS

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ATC Level 3

ANTIPSYCHOTICS

2

DIGESTIVES, INCL. ENZYMES

1

I.V. SOLUTION ADDITIVES

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OTHER DERMATOLOGICAL PREPARATIONS

1

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ATC Level 4

Lithium

2

Acid preparations

1

Electrolyte solutions

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Other dermatologicals

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Substance Form

Salts, Hydrates, Esters, etc.

37

Principal Form

3

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SULFATE ION

7IS9N8KPMG

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Status:

US Approved Rx (2023)

First marketed in 1921

Class (Stereo):

CHEMICAL (ACHIRAL)

Conditions:

SULFATE (as sodium sulfate, potassium sulfate, and magnesium sulfate) is a component of SUPREP Bowel Prep Kit. It is an osmotic laxative indicated for cleansing of the colon in preparation for colonoscopy in adults. Sulfate salts provide sulfate anio...

ns, which are poorly absorbed. The osmotic effect of unabsorbed sulfate anions and the associated cations causes water to be retained within the gastrointestinal tract. SUPREP Bowel Prep Kit, when ingested with a large volume of water, produces copious watery diarrhea.

LITHIUM CATION

8H8Z5UER66

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Status:

US Approved Rx (2009)

First marketed in 1921

Class (Stereo):

CHEMICAL (ACHIRAL)

Targets:

neurotrophin signaling pathway

Glycogen synthase kinase-3 beta

3'(2'),5'-bisphosphate nucleotidase 1

Glycogen synthase kinase-3 beta

Conditions:

Bipolar disorder, manic episodes

Lithium is an alkali metal widely used in industry. Lithium salts are indicated in the treatment of manic episodes of Bipolar Disorder. The use of lithium in psychiatry goes back to the mid-19th century. Early work, however, was soon forgotten, and J...

ohn Cade is credited with reintroducing lithium to psychiatry for mania in 1949. Mogens Schou undertook a randomly controlled trial for mania in 1954, and in the course of that study became curious about lithium as a prophylactic for depressive illness. In 1970, the United States became the 50th country to admit lithium to the marketplace. The specific mechanisms by which lithium exerts its mood-stabilizing effects are not well understood. Lithium appears to preserve or increase the volume of brain structures involved in emotional regulation such as the prefrontal cortex, hippocampus and amygdala, possibly reflecting its neuroprotective effects. At a neuronal level, lithium reduces excitatory (dopamine and glutamate) but increases inhibitory (GABA) neurotransmission; however, these broad effects are underpinned by complex neurotransmitter systems that strive to achieve homeostasis by way of compensatory changes. For example, at an intracellular and molecular level, lithium targets second-messenger systems that further modulate neurotransmission. For instance, the effects of lithium on the adenyl cyclase and phospho-inositide pathways, as well as protein kinase C, may serve to dampen excessive excitatory neurotransmission. In addition to these many putative mechanisms, it has also been proposed that the neuroprotective effects of lithium are key to its therapeutic actions. In this regard, lithium has been shown to reduce the oxidative stress that occurs with multiple episodes of mania and depression. Further, it increases protective proteins such as brain-derived neurotrophic factor and B-cell lymphoma 2, and reduces apoptotic processes through inhibition of glycogen synthase kinase 3 and autophagy.

Chloride ion

Q32ZN48698

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Status:

US Previously Marketed

First marketed in 1921

Class (Stereo):

CHEMICAL (ACHIRAL)

Conditions:

Surgical Blood Losses

HYDROCHLORIC ACID is formed by dissolving hydrogen chloride gas in water. It is a strong corrosive acid that is commonly used as a laboratory reagent. Also, it constitutes the majority of gastric acid, the human digestive fluid. Skin contact with HYD...

ROCHLORIC ACID can cause redness, pain, and severe skin burns. It may cause severe burns to the eye and permanent eye damage.

LITHIUM IODIDE TRIHYDRATE

PS8215OJNR

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Status:

US Approved Rx (2009)

First marketed in 1921

Class (Stereo):

CHEMICAL (ACHIRAL)

Targets:

neurotrophin signaling pathway

Glycogen synthase kinase-3 beta

3'(2'),5'-bisphosphate nucleotidase 1

Glycogen synthase kinase-3 beta

Conditions:

Bipolar disorder, manic episodes

Lithium is an alkali metal widely used in industry. Lithium salts are indicated in the treatment of manic episodes of Bipolar Disorder. The use of lithium in psychiatry goes back to the mid-19th century. Early work, however, was soon forgotten, and J...

ohn Cade is credited with reintroducing lithium to psychiatry for mania in 1949. Mogens Schou undertook a randomly controlled trial for mania in 1954, and in the course of that study became curious about lithium as a prophylactic for depressive illness. In 1970, the United States became the 50th country to admit lithium to the marketplace. The specific mechanisms by which lithium exerts its mood-stabilizing effects are not well understood. Lithium appears to preserve or increase the volume of brain structures involved in emotional regulation such as the prefrontal cortex, hippocampus and amygdala, possibly reflecting its neuroprotective effects. At a neuronal level, lithium reduces excitatory (dopamine and glutamate) but increases inhibitory (GABA) neurotransmission; however, these broad effects are underpinned by complex neurotransmitter systems that strive to achieve homeostasis by way of compensatory changes. For example, at an intracellular and molecular level, lithium targets second-messenger systems that further modulate neurotransmission. For instance, the effects of lithium on the adenyl cyclase and phospho-inositide pathways, as well as protein kinase C, may serve to dampen excessive excitatory neurotransmission. In addition to these many putative mechanisms, it has also been proposed that the neuroprotective effects of lithium are key to its therapeutic actions. In this regard, lithium has been shown to reduce the oxidative stress that occurs with multiple episodes of mania and depression. Further, it increases protective proteins such as brain-derived neurotrophic factor and B-cell lymphoma 2, and reduces apoptotic processes through inhibition of glycogen synthase kinase 3 and autophagy.

LITHIUM IODIDE

S6K2XET783

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Status:

US Approved Rx (2009)

First marketed in 1921

Class (Stereo):

CHEMICAL (ACHIRAL)

Targets:

neurotrophin signaling pathway

Glycogen synthase kinase-3 beta

3'(2'),5'-bisphosphate nucleotidase 1

Glycogen synthase kinase-3 beta

Conditions:

Bipolar disorder, manic episodes

Lithium is an alkali metal widely used in industry. Lithium salts are indicated in the treatment of manic episodes of Bipolar Disorder. The use of lithium in psychiatry goes back to the mid-19th century. Early work, however, was soon forgotten, and J...

ohn Cade is credited with reintroducing lithium to psychiatry for mania in 1949. Mogens Schou undertook a randomly controlled trial for mania in 1954, and in the course of that study became curious about lithium as a prophylactic for depressive illness. In 1970, the United States became the 50th country to admit lithium to the marketplace. The specific mechanisms by which lithium exerts its mood-stabilizing effects are not well understood. Lithium appears to preserve or increase the volume of brain structures involved in emotional regulation such as the prefrontal cortex, hippocampus and amygdala, possibly reflecting its neuroprotective effects. At a neuronal level, lithium reduces excitatory (dopamine and glutamate) but increases inhibitory (GABA) neurotransmission; however, these broad effects are underpinned by complex neurotransmitter systems that strive to achieve homeostasis by way of compensatory changes. For example, at an intracellular and molecular level, lithium targets second-messenger systems that further modulate neurotransmission. For instance, the effects of lithium on the adenyl cyclase and phospho-inositide pathways, as well as protein kinase C, may serve to dampen excessive excitatory neurotransmission. In addition to these many putative mechanisms, it has also been proposed that the neuroprotective effects of lithium are key to its therapeutic actions. In this regard, lithium has been shown to reduce the oxidative stress that occurs with multiple episodes of mania and depression. Further, it increases protective proteins such as brain-derived neurotrophic factor and B-cell lymphoma 2, and reduces apoptotic processes through inhibition of glycogen synthase kinase 3 and autophagy.

LITHIUM HYDRIDE

68KF447EX3

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Status:

US Approved Rx (2009)

First marketed in 1921

Class (Stereo):

CHEMICAL (ACHIRAL)

Targets:

neurotrophin signaling pathway

Glycogen synthase kinase-3 beta

3'(2'),5'-bisphosphate nucleotidase 1

Glycogen synthase kinase-3 beta

Conditions:

Bipolar disorder, manic episodes

Lithium is an alkali metal widely used in industry. Lithium salts are indicated in the treatment of manic episodes of Bipolar Disorder. The use of lithium in psychiatry goes back to the mid-19th century. Early work, however, was soon forgotten, and J...

ohn Cade is credited with reintroducing lithium to psychiatry for mania in 1949. Mogens Schou undertook a randomly controlled trial for mania in 1954, and in the course of that study became curious about lithium as a prophylactic for depressive illness. In 1970, the United States became the 50th country to admit lithium to the marketplace. The specific mechanisms by which lithium exerts its mood-stabilizing effects are not well understood. Lithium appears to preserve or increase the volume of brain structures involved in emotional regulation such as the prefrontal cortex, hippocampus and amygdala, possibly reflecting its neuroprotective effects. At a neuronal level, lithium reduces excitatory (dopamine and glutamate) but increases inhibitory (GABA) neurotransmission; however, these broad effects are underpinned by complex neurotransmitter systems that strive to achieve homeostasis by way of compensatory changes. For example, at an intracellular and molecular level, lithium targets second-messenger systems that further modulate neurotransmission. For instance, the effects of lithium on the adenyl cyclase and phospho-inositide pathways, as well as protein kinase C, may serve to dampen excessive excitatory neurotransmission. In addition to these many putative mechanisms, it has also been proposed that the neuroprotective effects of lithium are key to its therapeutic actions. In this regard, lithium has been shown to reduce the oxidative stress that occurs with multiple episodes of mania and depression. Further, it increases protective proteins such as brain-derived neurotrophic factor and B-cell lymphoma 2, and reduces apoptotic processes through inhibition of glycogen synthase kinase 3 and autophagy.

AMMONIUM BISULFATE

6218R7MBZB

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Status:

US Approved Rx (2023)

First marketed in 1921

Class (Stereo):

CHEMICAL (ACHIRAL)

Conditions:

SULFATE (as sodium sulfate, potassium sulfate, and magnesium sulfate) is a component of SUPREP Bowel Prep Kit. It is an osmotic laxative indicated for cleansing of the colon in preparation for colonoscopy in adults. Sulfate salts provide sulfate anio...

ns, which are poorly absorbed. The osmotic effect of unabsorbed sulfate anions and the associated cations causes water to be retained within the gastrointestinal tract. SUPREP Bowel Prep Kit, when ingested with a large volume of water, produces copious watery diarrhea.

LITHIUM GLUCONATE

29L5I58185

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Status:

US Approved Rx (2009)

First marketed in 1921

Class (Stereo):

CHEMICAL (ABSOLUTE)

Targets:

neurotrophin signaling pathway

Glycogen synthase kinase-3 beta

3'(2'),5'-bisphosphate nucleotidase 1

Glycogen synthase kinase-3 beta

Conditions:

Bipolar disorder, manic episodes

Lithium is an alkali metal widely used in industry. Lithium salts are indicated in the treatment of manic episodes of Bipolar Disorder. The use of lithium in psychiatry goes back to the mid-19th century. Early work, however, was soon forgotten, and J...

ohn Cade is credited with reintroducing lithium to psychiatry for mania in 1949. Mogens Schou undertook a randomly controlled trial for mania in 1954, and in the course of that study became curious about lithium as a prophylactic for depressive illness. In 1970, the United States became the 50th country to admit lithium to the marketplace. The specific mechanisms by which lithium exerts its mood-stabilizing effects are not well understood. Lithium appears to preserve or increase the volume of brain structures involved in emotional regulation such as the prefrontal cortex, hippocampus and amygdala, possibly reflecting its neuroprotective effects. At a neuronal level, lithium reduces excitatory (dopamine and glutamate) but increases inhibitory (GABA) neurotransmission; however, these broad effects are underpinned by complex neurotransmitter systems that strive to achieve homeostasis by way of compensatory changes. For example, at an intracellular and molecular level, lithium targets second-messenger systems that further modulate neurotransmission. For instance, the effects of lithium on the adenyl cyclase and phospho-inositide pathways, as well as protein kinase C, may serve to dampen excessive excitatory neurotransmission. In addition to these many putative mechanisms, it has also been proposed that the neuroprotective effects of lithium are key to its therapeutic actions. In this regard, lithium has been shown to reduce the oxidative stress that occurs with multiple episodes of mania and depression. Further, it increases protective proteins such as brain-derived neurotrophic factor and B-cell lymphoma 2, and reduces apoptotic processes through inhibition of glycogen synthase kinase 3 and autophagy.

LITHIUM ASPARTATE MONOHYDRATE

1BJG19P0NX

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Status:

US Approved Rx (2009)

First marketed in 1921

Class (Stereo):

CHEMICAL (ABSOLUTE)

Targets:

neurotrophin signaling pathway

Glycogen synthase kinase-3 beta

3'(2'),5'-bisphosphate nucleotidase 1

Glycogen synthase kinase-3 beta

Conditions:

Bipolar disorder, manic episodes

Lithium is an alkali metal widely used in industry. Lithium salts are indicated in the treatment of manic episodes of Bipolar Disorder. The use of lithium in psychiatry goes back to the mid-19th century. Early work, however, was soon forgotten, and J...

ohn Cade is credited with reintroducing lithium to psychiatry for mania in 1949. Mogens Schou undertook a randomly controlled trial for mania in 1954, and in the course of that study became curious about lithium as a prophylactic for depressive illness. In 1970, the United States became the 50th country to admit lithium to the marketplace. The specific mechanisms by which lithium exerts its mood-stabilizing effects are not well understood. Lithium appears to preserve or increase the volume of brain structures involved in emotional regulation such as the prefrontal cortex, hippocampus and amygdala, possibly reflecting its neuroprotective effects. At a neuronal level, lithium reduces excitatory (dopamine and glutamate) but increases inhibitory (GABA) neurotransmission; however, these broad effects are underpinned by complex neurotransmitter systems that strive to achieve homeostasis by way of compensatory changes. For example, at an intracellular and molecular level, lithium targets second-messenger systems that further modulate neurotransmission. For instance, the effects of lithium on the adenyl cyclase and phospho-inositide pathways, as well as protein kinase C, may serve to dampen excessive excitatory neurotransmission. In addition to these many putative mechanisms, it has also been proposed that the neuroprotective effects of lithium are key to its therapeutic actions. In this regard, lithium has been shown to reduce the oxidative stress that occurs with multiple episodes of mania and depression. Further, it increases protective proteins such as brain-derived neurotrophic factor and B-cell lymphoma 2, and reduces apoptotic processes through inhibition of glycogen synthase kinase 3 and autophagy.

LITHIUM CITRATE ANHYDROUS

3655633623

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Status:

US Approved Rx (2009)

First marketed in 1921

Class (Stereo):

CHEMICAL (ACHIRAL)

Targets:

neurotrophin signaling pathway

Glycogen synthase kinase-3 beta

3'(2'),5'-bisphosphate nucleotidase 1

Glycogen synthase kinase-3 beta

Conditions:

Bipolar disorder, manic episodes

Lithium is an alkali metal widely used in industry. Lithium salts are indicated in the treatment of manic episodes of Bipolar Disorder. The use of lithium in psychiatry goes back to the mid-19th century. Early work, however, was soon forgotten, and J...

ohn Cade is credited with reintroducing lithium to psychiatry for mania in 1949. Mogens Schou undertook a randomly controlled trial for mania in 1954, and in the course of that study became curious about lithium as a prophylactic for depressive illness. In 1970, the United States became the 50th country to admit lithium to the marketplace. The specific mechanisms by which lithium exerts its mood-stabilizing effects are not well understood. Lithium appears to preserve or increase the volume of brain structures involved in emotional regulation such as the prefrontal cortex, hippocampus and amygdala, possibly reflecting its neuroprotective effects. At a neuronal level, lithium reduces excitatory (dopamine and glutamate) but increases inhibitory (GABA) neurotransmission; however, these broad effects are underpinned by complex neurotransmitter systems that strive to achieve homeostasis by way of compensatory changes. For example, at an intracellular and molecular level, lithium targets second-messenger systems that further modulate neurotransmission. For instance, the effects of lithium on the adenyl cyclase and phospho-inositide pathways, as well as protein kinase C, may serve to dampen excessive excitatory neurotransmission. In addition to these many putative mechanisms, it has also been proposed that the neuroprotective effects of lithium are key to its therapeutic actions. In this regard, lithium has been shown to reduce the oxidative stress that occurs with multiple episodes of mania and depression. Further, it increases protective proteins such as brain-derived neurotrophic factor and B-cell lymphoma 2, and reduces apoptotic processes through inhibition of glycogen synthase kinase 3 and autophagy.

Showing 1 - 10 of 40 results

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