Background and Purpose3‐Iodothyronamine (3‐T1AM) is an endogenous thyroid hormone derivative reported to induce strong hypothermia and bradycardia within minutes upon injection in rodents. Although 3‐T1AM is rapidly converted to several other metabolites in vivo, these strong pharmacological responses were solely attributed to 3‐T1AM, leaving potential contributions of downstream products untested. We therefore examined the cardiometabolic effects of 3‐iodothyroacetic acid (TA1), the main degradation product of 3‐T1AM.Experimental ApproachWe used a sensitive implantable radiotelemetry system in C57/Bl6J mice to study the effects of TA1 on body temperature and heart rate, as well as other metabolic parameters.Key ResultsInterestingly, despite using pharmacological TA1 doses, we observed no effects on heart rate or body temperature after a single TA1 injection (50 mg·kg−1, i.p.) compared to sham‐injected controls. Repeated administration of TA1 (5 mg·kg−1, i.p. for 7 days) likewise did not alter body weight, food and water intake, heart rate, blood pressure, brown adipose tissue (BAT) thermogenesis or body temperature. Moreover, mRNA expression of tissue specific genes in heart, kidney, liver, BAT and lung was also not altered by TA1 compared to sham‐injected controls.Conclusions and ImplicationsOur data therefore conclusively demonstrate that TA1 does not contribute to the cardiovascular or thermoregulatory effects observed after 3‐T1AM administration in mice, suggesting that the oxidative deamination constitutes an important deactivation mechanism for 3‐T1AM with possible implications for cardiovascular and thermoregulatory functions.