更新于：2024-11-01

TPO x THR-α x THR-β

更新于：2024-11-01

基本信息

关联

项与 TPO x THR-α x THR-β 相关的药物

Liothyronine sodium/Thiamazole

碘塞罗宁钠/甲巯咪唑

靶点

THR-α x THR-β x TPO

作用机制

THR-α激动剂 [+2]

在研机构

Abbott Laboratories [+1]

原研机构

Musli Thyropeutics Ltd.

在研适应症

胶质母细胞瘤

非在研适应症-

最高研发阶段临床2期

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 TPO x THR-α x THR-β 相关的临床结果

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100 项与 TPO x THR-α x THR-β 相关的转化医学

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0 项与 TPO x THR-α x THR-β 相关的专利（医药）

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项与 TPO x THR-α x THR-β 相关的文献（医药）

2023-04-01·Science of The Total Environment

An integrative investigation of developmental toxicities induced by triphenyltin in a larval coral reef fish, Amphiprion ocellaris

Article

作者: Liang, Zhi-Fang ; Cai, Xing-Wei ; Zhang, Ji-Liang ; Diao, Xiao-Ping ; Hou, Yu ; Duan, Dan-Dan

Triphenyltin (TPT) is widely distributed on coastlines, which makes coral reef fish a potential target of TPT pollution. However, the negative effects of TPT on coral reef fish remain poorly understood. Therefore, in the present study, the larval coral reef fish Amphiprion ocellaris was used to investigate the developmental toxicities of TPT at environmentally relevant concentrations (0, 1, 10 and 100 ng/L). After TPT exposure for 14 d, the cumulative mortality increased, and growth was suppressed. In addition, TPT exposure inhibited the development of melanophores and xanthophores and delayed white strip formation, which might be responsible for the disruption of the genes (erbb3b, mitfa, kit, xdh, tyr, oca2, itk and trim33) related to pigmentation. TPT exposure also attenuated ossification of head skeletal elements and the vertebral column and inhibited the expression of genes (bmp2, bmp4 and sp7) related to skeletal development. The observed developmental toxicities on growth, pigmentation and skeleton development might be associated with the disruption of thyroid hormones and the genes related to thyroid hormone regulation (tshβ, thrα, thrβ, tg, tpo, dio2, and ttr). In addition, TPT exposure interfered with locomotor and shoaling behavior, and the related genes dbh, avp and avpr1aa. Taken together, our results suggest that TPT pollution might threaten the development of one of the most iconic coral reef fish, which might produce disastrous consequences on the health of coral reef ecosystems.

2022-04-01·European Thyroid Journal4区 · 医学

Tissue sensitivity to thyroid hormones may change over time

4区 · 医学

Article

作者: Persani, Luca ; De Filippis, Tiziana ; Rigon, Franco ; Salvatoni, Alessandro ; Guizzardi, Fabiana ; Radetti, Giorgio ; Bonomi, Marco ; Cirello, Valentina ; Campi, Irene ; Longhi, Silvia

IntroductionPatients with congenital hypothyroidism (CH) may transiently show a certain degree of pituitary resistance to levothyroxine (LT4) which, however, normalizes subsequently. However, in some individuals, thyroid-stimulating hormone (TSH) fails to normalize despite adequate LT4 treatment.MethodsNine patients with CH followed in three Academic Centre who developed over time resistance to thyroid hormones underwent extensive biochemical and genetic analyses. These latter were performed by Sanger sequence or targeted next-generation sequencing technique including a panel of candidate genes involved in thyroid hormone actions and congenital hypothyroidism (CH): THRA, THRB, DIO1, DIO2, SLC16A2, SECISBP2, DUOX2, DUOXA2, FOXE1, GLIS3, IYD, JAG1, NKX2-1, NKX2-5, PAX8, SLC26A4, SLC5A5, TG, TPO, TSHR.ResultsAll patients displayed a normal sensitivity to thyroid hormone (TH) in the first years of life but developed variable degrees of resistance to LT4 treatment at later stages. In all cases, TSH normalized only in the presence of high free thyroxine levels. Tri-iodothyronine suppression test followed by thyrotrophin-releasing hormone stimulation was performed in two cases and was compatible with central resistance to THs. This biochemical feature was present independently on the cause of CH, being observed either in patients with an ectopic (n = 2) or eutopic gland (n = 3) or in case of athyreosis (n = 1). None of the patients had genetic variants in genes involved in the regulation of TH actions, while in two cases, we found two double heterozygous missense variants in TSHR and GLIS3 or in DUOX2 and SLC26A4 genes, respectively.ConclusionsWe report CH patients who showed an acquired and unexplainable pituitary refractoriness to TH action.

2010-06-01·The Journal of Clinical Endocrinology & Metabolism2区 · 医学

Genistein Aglycone Does Not Affect Thyroid Function: Results from a Three-Year, Randomized, Double-Blind, Placebo-Controlled Trial

2区 · 医学

Article

作者: Marini, Herbert ; Adamo, Elena Bianca ; Atteritano, Marco ; Minutoli, Letteria ; Polito, Francesca ; Bitto, Alessandra ; Mazzaferro, Susanna ; Altavilla, Domenica ; Granese, Roberta ; Squadrito, Francesco ; Corrado, Francesco ; D'Anna, Rosario ; Russo, Silvia

AbstractContext and Objective: Genistein aglycone positively affects postmenopausal symptoms. However, questions about its long-term safety on the thyroid gland still remain.Design: The parent study was a randomized, double-blind, placebo-controlled trial involving 389 osteopenic, postmenopausal women for 24 months. A subcohort (138 patients) continued therapy for an additional year.Setting: Patients received ambulatory care.Patients and Interventions: Participants received 54 mg of genistein aglycone daily (n = 71) or placebo (n = 67), plus calcium and vitamin D3 at therapeutic doses. Circulating thyroid hormones (TSH, free T3, free T4) and autoantibodies (thyroid peroxidase, thyroglobulin, and thyroid microsomal antigen) were assessed in 40 genistein and 37 placebo subjects who completed 3 yr. Thyroid hormone receptor (THRα and THRβ) and retinoid receptor (RARα, RARγ, and RXRα) expression from peripheral blood monocytes was also evaluated at baseline, 12, 24, and 36 months in all 3-yr completers.Results: Genistein administration over 3 yr did not affect serum thyroid hormones or autoantibodies. In addition, there were no differences in THRα, THRβ, RARα, RARγ, or RXRα mRNA expression between groups.Conclusion: These data suggest that genistein aglycone intake does not significantly increase the risk of clinical or subclinical hypothyroidism at the dose of 54 mg/d.