Approval Year
Substance Class |
Protein
Created
by
admin
on
Edited
Sat Dec 16 12:03:50 GMT 2023
by
admin
on
Sat Dec 16 12:03:50 GMT 2023
|
Protein Type | RECEPTOR |
Protein Sub Type | HYDROXYTRYPTAMINE RECEPTOR |
Sequence Origin | HUMAN |
Sequence Type | COMPLETE |
Record UNII |
6E2Z4UWILI
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Record Status |
Validated (UNII)
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Record Version |
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-
Download
Name | Type | Language | ||
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Common 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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P41595
Created by
admin on Sat Dec 16 12:03:52 GMT 2023 , Edited by admin on Sat Dec 16 12:03:52 GMT 2023
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PRIMARY | |||
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6E2Z4UWILI
Created by
admin on Sat Dec 16 12:03:52 GMT 2023 , Edited by admin on Sat Dec 16 12:03:52 GMT 2023
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PRIMARY |
From | To |
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1_128 | 1_207 |
1_350 | 1_353 |
Glycosylation Type | HUMAN |
Glycosylation Link Type | Site |
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N | 1_30 |
Related Record | Type | Details | ||
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PARTIAL AGONIST->TARGET |
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INHIBITOR -> TARGET |
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AGONIST -> TARGET |
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AGONIST -> TARGET |
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INHIBITOR -> TARGET |
Ki
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PARTIAL AGONIST->TARGET |
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INHIBITOR -> TARGET |
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AGONIST->OFF-TARGET |
5-HT2B receptors, which were subsequently identified as the target for cardiac valvulopathy and pulmonary hypertension. Release of serotonin leads to 5-HT2B signaling.
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WEAK AGONIST->OFF TARGET |
Ki
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RADIOLIGAND->TARGET |
Ki
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AGONIST -> TARGET |
Eletriptan binds with high affinity to 5-HT1B, 5-HT1D and 5-HT1F receptors, has modest affinity for 5-HT1A, 5-HT1E, 5-HT2B and 5-HT7 receptors
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INHIBITOR -> TARGET |
Acts as a mixed antagonist for the 5-HT2B and 5-HT2C serotonin receptors, with good selectivity over other serotonin receptor subtypes and slight preference for 5-HT2C over 5-HT2B.
ANTAGONIST
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AGONIST -> TARGET |
A full agonist.
Ki
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INHIBITOR -> TARGET |
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AGONIST -> TARGET |
BINDING
IC50
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INHIBITOR -> TARGET |
ANTAGONIST
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PARTIAL AGONIST->TARGET | |||
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INHIBITOR -> TARGET |
Ki
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INHIBITOR -> TARGET |
BINDING
IC50
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INHIBITOR -> TARGET |
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INHIBITOR -> TARGET |
ANTAGONIST
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INVERSE AGONIST->TARGET |
IC50
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AGONIST -> TARGET |
BINDING
IC50
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INVERSE AGONIST->TARGET |
Ki
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INHIBITOR -> TARGET |
Ki
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INHIBITOR -> TARGET |
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AGONIST -> TARGET |
Ki
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AGONIST -> TARGET |
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AGONIST -> TARGET | |||
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INHIBITOR -> TARGET |
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AGONIST -> TARGET | |||
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WEAK AGONIST->OFF TARGET |
Emax,40%
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AGONIST -> TARGET |
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INHIBITOR -> TARGET |
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AGONIST->OFF-TARGET |
5-HT2B receptors, which were subsequently identified as the target for cardiac valvulopathy and pulmonary hypertension. Release of serotonin leads to 5-HT2B signaling.
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INHIBITOR -> TARGET |
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AGONIST -> TARGET |
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AGONIST -> TARGET |
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AGONIST -> TARGET |
Ki
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INHIBITOR -> TARGET |
Ki
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RADIOLIGAND->TARGET |
Kd
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INHIBITOR -> TARGET |
ANTAGONIST
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AGONIST->OFF-TARGET |
Responsible for valvular heart disease (VHD) with the administration of phentermine and fenfluramine (phen/fen) and dexfenfluramine1 led to the withdrawal of fenfluramine and dexfenfluramine from the marketplace in September 1997.
Ki
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AGONIST->OFF-TARGET |
We propose that preferential stimulation of valvular 5-HT2B receptors by norfenfluramine, ergot drugs, or 5-HT released from carcinoid tumors (with
or without accompanying 5-HT2A receptor activation) may contribute to valvular fibroplasia in humans.
Ki
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AGONIST->OFF-TARGET |
Indeed all drugs and drug metabolites that induce heart valvular disease in humans activate 5-HT2B receptors in vivo and in vitro and this activity is thought to be important for the development of fibrotic lesions upon chronic human administration.
Ki
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AGONIST -> TARGET |
Ki
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Name | Property Type | Amount | Referenced Substance | Defining | Parameters | References |
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Molecular Formula | CHEMICAL |
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MOL_WEIGHT | CHEMICAL |
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