Approval Year
| Substance Class |
Protein
Created
by
admin
on
Edited
Tue Apr 01 22:16:40 GMT 2025
by
admin
on
Tue Apr 01 22:16:40 GMT 2025
|
| Protein Sub Type | |
| Sequence Origin | HUMAN |
| Sequence Type | COMPLETE |
| Record UNII |
DHD0GV07RG
|
| Record Status |
Validated (UNII)
|
| Record Version |
|
-
Download
| Name | Type | Language | ||
|---|---|---|---|---|
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Common Name | English | ||
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Preferred Name | English | ||
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Common Name | English | ||
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Common Name | English |
| Code System | Code | Type | Description | ||
|---|---|---|---|---|---|
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O95832
Created by
admin on Tue Apr 01 22:16:40 GMT 2025 , Edited by admin on Tue Apr 01 22:16:40 GMT 2025
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PRIMARY | |||
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DHD0GV07RG
Created by
admin on Tue Apr 01 22:16:40 GMT 2025 , Edited by admin on Tue Apr 01 22:16:40 GMT 2025
|
PRIMARY |
| From | To |
|---|---|
| 1_54 | 1_64 |
| Glycosylation Link Type | Site |
|---|---|
| N | 1_72 |
| Related Record | Type | Details | ||
|---|---|---|---|---|
|
LIGAND->TARGET |
The nonclinical profile of ALE.F02 supports its potential as a treatment for advanced liver
fibrosis. In vitro, ALE.F02 has displayed a highly specific binding affinity for CLDN1.
Treatment by ALE.F02 was correlated with significant down-regulation of the expression of key
fibrosis promoting signaling pathways as well as the suppression of gene expression linked to the
Ras/Raf/MEK/ERK signaling pathways in human liver tissue ex vivo; these pathways are
hypothesized to play an important role in liver fibrosis. In diet-induced liver fibrosis in
humanized mice,
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| Name | Property Type | Amount | Referenced Substance | Defining | Parameters | References |
|---|---|---|---|---|---|---|
| MOL_WEIGHT:NUMBER(CALCULATED) | CHEMICAL |
|