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US Approved Rx

30

US Approved OTC

10

Other

3

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Primary Target

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

30

Glycogen synthase kinase-3 beta

30

neurotrophin signaling pathway

30

Sodium channel alpha subunit

10

Sodium/potassium-transporting ATPase

10

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Highest Phase

Approved

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Approval Year

1921

40

Unknown

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Condition

Bipolar disorder, manic episodes

30

Genital warts

10

Hyperkalemia

10

Molluscum contagiosum

10

Nail grooves

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Treatment Modality

Primary

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CNS Activity

CNS Active

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CNS Penetrant

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Originator

Arfvedson, J.A.

30

Davy, H.

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Substance Class

Chemical

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CAS

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FDA UNII

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PUBCHEM

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EPA CompTox

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ECHA (EC/EINECS)

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ATC Level 1

NERVOUS SYSTEM

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DERMATOLOGICALS

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SENSORY ORGANS

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ATC Level 2

PSYCHOLEPTICS

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OPHTHALMOLOGICALS

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OTHER DERMATOLOGICAL PREPARATIONS

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ATC Level 3

ANTIPSYCHOTICS

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OTHER DERMATOLOGICAL PREPARATIONS

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OTHER OPHTHALMOLOGICALS

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ATC Level 4

Lithium

2

Other dermatologicals

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Other ophthalmologicals

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Substance Form

Salts, Hydrates, Esters, etc.

38

Principal Form

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Showing 1 - 10 of 43 results

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LITHIUM CATION

8H8Z5UER66

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Status:

US Approved Rx (1986)

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.

HYDROXIDE ION

9159UV381P

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Status:

US Approved OTC

First marketed in 1921

Class (Stereo):

CHEMICAL (ACHIRAL)

Targets:

Sodium/potassium-transporting ATPase

Sodium channel alpha subunit

Conditions:

Molluscum contagiosum

Sodium is the primary cation (positive ion) in extracellular fluids in animals and humans. Sodium ions are necessary for regulation of blood and body fluids, transmission of nerve impulses, heart activity, and certain metabolic functions. Physiologic...

ally, it exists as an ion in the body. Sodium is needed by animals, which maintain high concentrations in their blood and extracellular fluids, but the ion is not needed by plants. The human requirement for sodium in the diet is less than 500 mg per day, which is typically less than a tenth as much as many diets "seasoned to taste. " Most people consume far more sodium than is physiologically needed. For certain people with salt-sensitive blood pressure, this extra intake may cause a negative effect on health.

N-METHYLMALEIMIDE

P0TFZ8R21Y

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Status:

Other

Class (Stereo):

CHEMICAL (ACHIRAL)

LITHIUM ALUMINUM HYDRIDE

77UJC875H4

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Status:

Other

Class (Stereo):

CHEMICAL (ACHIRAL)

METHYL ANISATE

2MFL7873W9

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Status:

Other

Class (Stereo):

CHEMICAL (ACHIRAL)

LITHIUM IODIDE TRIHYDRATE

PS8215OJNR

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Status:

US Approved Rx (1986)

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 (1986)

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 (1986)

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 GLUCONATE

29L5I58185

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Status:

US Approved Rx (1986)

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 (1986)

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.

Showing 1 - 10 of 43 results

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