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Names | |
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Preferred IUPAC name
4-[4-(2-Aminoethyl)-2-iodophenoxy]phenol | |
Other names
T1AM
| |
Identifiers | |
3D model (
JSmol)
|
|
ChemSpider | |
ECHA InfoCard | 100.211.501 |
PubChem
CID
|
|
CompTox Dashboard (
EPA)
|
|
| |
| |
Properties | |
C14H14INO2 | |
Molar mass | 355.17 g/mol |
Except where otherwise noted, data are given for materials in their
standard state (at 25 °C [77 °F], 100 kPa).
|
3-Iodothyronamine (T1AM) is an endogenous thyronamine. T1AM is a high-affinity ligand for the trace amine-associated receptor TAAR1 (TAR1, TA1), a recently discovered G protein-coupled receptor. [1] [2] T1AM is the most potent endogenous TAAR1 agonist yet discovered. [3] Activation of TAAR1 by T1AM results in the production of large amounts of cAMP. This effect is coupled with decreased body temperature and cardiac output. [4] Wu et al. have pointed out that this relationship is not typical of the endocrine system, indicating that TAAR1 activity may not be coupled to G-proteins in some tissues, or that T1AM may interact with other receptor subtypes. [3]
T1AM may be part of a signaling pathway to modulate cardiac function, as the compound can induce negative inotropic effects and decrease cardiac output. [5]
![]() | |
![]() | |
Names | |
---|---|
Preferred IUPAC name
4-[4-(2-Aminoethyl)-2-iodophenoxy]phenol | |
Other names
T1AM
| |
Identifiers | |
3D model (
JSmol)
|
|
ChemSpider | |
ECHA InfoCard | 100.211.501 |
PubChem
CID
|
|
CompTox Dashboard (
EPA)
|
|
| |
| |
Properties | |
C14H14INO2 | |
Molar mass | 355.17 g/mol |
Except where otherwise noted, data are given for materials in their
standard state (at 25 °C [77 °F], 100 kPa).
|
3-Iodothyronamine (T1AM) is an endogenous thyronamine. T1AM is a high-affinity ligand for the trace amine-associated receptor TAAR1 (TAR1, TA1), a recently discovered G protein-coupled receptor. [1] [2] T1AM is the most potent endogenous TAAR1 agonist yet discovered. [3] Activation of TAAR1 by T1AM results in the production of large amounts of cAMP. This effect is coupled with decreased body temperature and cardiac output. [4] Wu et al. have pointed out that this relationship is not typical of the endocrine system, indicating that TAAR1 activity may not be coupled to G-proteins in some tissues, or that T1AM may interact with other receptor subtypes. [3]
T1AM may be part of a signaling pathway to modulate cardiac function, as the compound can induce negative inotropic effects and decrease cardiac output. [5]