Inxight Drugs

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

National Institutes of Health Divider Arrow

NCATS

Return Home Inxight Drugs

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

Show Filters

Hide Filters

Primary Target

interleukin-10 secretion

2

Histamine H1 receptor

315

Dopamine D2 receptor

297

DNA

278

Bacterial penicillin-binding protein

233

All Match

Any Match

Exclude Selected

Exclude Selected

Development Status

Investigational

2

All Match

Any Match

Exclude Selected

Exclude Selected

Approval Year

Unknown

2

All Match

Any Match

Exclude Selected

Exclude Selected

Substance Class

Chemical

2

All Match

Any Match

Exclude Selected

Exclude Selected

Code System

CAS

2

CHEBI

2

EPA CompTox

2

FDA UNII

2

NSC

2

All Match

Any Match

Exclude Selected

Exclude Selected

Substance Form

Principal Form

1

Salts, Hydrates, Esters, etc.

1

All Match

Any Match

Exclude Selected

Exclude Selected

Showing 1 - 2 of 2 results

First page disabled
Previous page disabled
1
Next page disabled
Next page disabled

CIS-UROCANIC ACID

5LM7WD7VIC

Export Data
Search for Structure

Status:

Investigational

Class (Stereo):

CHEMICAL (ACHIRAL)

Targets:

Serotonin 2a (5-HT2a) receptor

interleukin-10 secretion

mast cell degranulation

GABA-A receptor; anion channel

Urocanic acid is a breakdown (deamination) product of histidine. In the liver, urocanic acid is an intermediate in the conversion of histidine to glutamic acid, whereas in the epidermis, it accumulates and may be both a UV protectant and an immunoreg...

ulator. Urocanic acid (UA) exists as a trans isomer (t-UA, approximately 30 mg/cm2) in the uppermost layer of the skin (stratum corneum). t-UA is formed as the cells of the second layer of skin become metabolically inactive. During this process, proteins and membranes degrade, histidine is released, and histidase (histidine ammonia lyase) catalyzes the deamination of histidine to form t-UA. t-UA accumulates in the epidermis until removal by either the monthly skin renewal cycle or sweat. Upon absorption of UV light, the naturally occurring t-UA isomerizes to its cis form, c-UA. Because DNA lesions (e. g. , pyrimidine dimers) in the lower epidermis can result from UV-B absorption, initial research proposed that t-UA acted as a natural sunscreen absorbing UV-B in the stratum corneum before the damaging rays could penetrate into lower epidermal zones. c-UA also suppresses contact hypersensitivity and delayed hypersensitivity, reduces the Langerhans cell count in the epidermis, prolongs skin-graft survival time, and affects natural killer cell activity. It has also been proposed that c-UA may mediate the transient alteration in immune surveillance resulting in immunosuppression induced after UV-irradiation, by interacting with immune cells locally and/or systemically to generate T cells with suppressor function.

UROCANIC ACID

G8D26XJJ3B

Export Data
Search for Structure

Status:

Investigational

Class (Stereo):

CHEMICAL (ACHIRAL)

Targets:

Serotonin 2a (5-HT2a) receptor

interleukin-10 secretion

mast cell degranulation

GABA-A receptor; anion channel

Urocanic acid is a breakdown (deamination) product of histidine. In the liver, urocanic acid is an intermediate in the conversion of histidine to glutamic acid, whereas in the epidermis, it accumulates and may be both a UV protectant and an immunoreg...

ulator. Urocanic acid (UA) exists as a trans isomer (t-UA, approximately 30 mg/cm2) in the uppermost layer of the skin (stratum corneum). t-UA is formed as the cells of the second layer of skin become metabolically inactive. During this process, proteins and membranes degrade, histidine is released, and histidase (histidine ammonia lyase) catalyzes the deamination of histidine to form t-UA. t-UA accumulates in the epidermis until removal by either the monthly skin renewal cycle or sweat. Upon absorption of UV light, the naturally occurring t-UA isomerizes to its cis form, c-UA. Because DNA lesions (e. g. , pyrimidine dimers) in the lower epidermis can result from UV-B absorption, initial research proposed that t-UA acted as a natural sunscreen absorbing UV-B in the stratum corneum before the damaging rays could penetrate into lower epidermal zones. c-UA also suppresses contact hypersensitivity and delayed hypersensitivity, reduces the Langerhans cell count in the epidermis, prolongs skin-graft survival time, and affects natural killer cell activity. It has also been proposed that c-UA may mediate the transient alteration in immune surveillance resulting in immunosuppression induced after UV-irradiation, by interacting with immune cells locally and/or systemically to generate T cells with suppressor function.

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