Inxight Drugs

U.S. Department of Health & Human Services Divider Arrow

National Institutes of Health Divider Arrow

NCATS

This repository is under review for potential modification in compliance with Administration directives.

Return Home Inxight Drugs

Home
Browse Drugs
Search
- Structure Search
- Sequence Search
Downloads
About

Show Filters

Hide Filters

Development Status

US Approved Rx

30

Other

3

US Previously Marketed

2

All Match

Any Match

Exclude Selected

Exclude Selected

Primary Target

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

30

Glycogen synthase kinase-3 beta

30

neurotrophin signaling pathway

30

All Match

Any Match

Exclude Selected

Exclude Selected

Highest Phase

Approved

32

All Match

Any Match

Exclude Selected

Exclude Selected

Approval Year

1921

32

Unknown

3

All Match

Any Match

Exclude Selected

Exclude Selected

Condition

Bipolar disorder, manic episodes

30

Surgical Blood Losses

2

All Match

Any Match

Exclude Selected

Exclude Selected

Treatment Modality

Primary

32

All Match

Any Match

Exclude Selected

Exclude Selected

CNS Activity

CNS Active

30

All Match

Any Match

Exclude Selected

Exclude Selected

Originator

Arfvedson, J.A.

30

All Match

Any Match

Exclude Selected

Exclude Selected

Substance Class

Chemical

35

All Match

Any Match

Exclude Selected

Exclude Selected

Code System

CAS

35

FDA UNII

35

PUBCHEM

35

EPA CompTox

33

SMS_ID

22

All Match

Any Match

Exclude Selected

Exclude Selected

ATC Level 1

NERVOUS SYSTEM

2

ALIMENTARY TRACT AND METABOLISM

1

BLOOD AND BLOOD FORMING ORGANS

1

DERMATOLOGICALS

1

All Match

Any Match

Exclude Selected

Exclude Selected

ATC Level 2

PSYCHOLEPTICS

2

BLOOD SUBSTITUTES AND PERFUSION SOLUTIONS

1

DIGESTIVES, INCL. ENZYMES

1

OTHER DERMATOLOGICAL PREPARATIONS

1

All Match

Any Match

Exclude Selected

Exclude Selected

ATC Level 3

ANTIPSYCHOTICS

2

DIGESTIVES, INCL. ENZYMES

1

I.V. SOLUTION ADDITIVES

1

OTHER DERMATOLOGICAL PREPARATIONS

1

All Match

Any Match

Exclude Selected

Exclude Selected

ATC Level 4

Lithium

2

Acid preparations

1

Electrolyte solutions

1

Other dermatologicals

1

All Match

Any Match

Exclude Selected

Exclude Selected

Substance Form

Salts, Hydrates, Esters, etc.

32

Principal Form

3

All Match

Any Match

Exclude Selected

Exclude Selected

Showing 1 - 10 of 35 results

First page disabled
Previous page disabled
1
Next page
Next page

LITHIUM CATION

8H8Z5UER66

Export Data
Search for Structure

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.

Sodium borohydride

87L0B9CPPA

Export Data
Search for Structure

Status:

Other

Class (Stereo):

CHEMICAL (ACHIRAL)

Chloride ion

Q32ZN48698

Export Data
Search for Structure

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

Export Data
Search for Structure

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

Export Data
Search for Structure

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

Export Data
Search for Structure

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 GLUCONATE

29L5I58185

Export Data
Search for Structure

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

Export Data
Search for Structure

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

Export Data
Search for Structure

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 SULFIDE

SW6C51V9JZ

Export Data
Search for Structure

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 35 results

First page disabled
Previous page disabled
1
Next page
Next page

HHS VULNERABILITY DISCLOSURE

For language access assistance, contact the NCATS Public Information Officer

National Center for Advancing Translational Sciences (NCATS),
6701 Democracy Boulevard, Bethesda MD 20892-4874 • 301-594-8966


			version 1.1