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levothyroxine sodium

✓ Approved

Institut Biochimique · TSHR · 小分子

什么是 levothyroxine sodium？

levothyroxine sodium 是一种小分子，由Institut Biochimique研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

公司Institut Biochimique
药物类别小分子
分子靶点TSHR
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Institut Biochimique

作用机制

分子靶点

levothyroxine sodium 作用于 1 个分子靶点：

TSHRthyroid stimulating hormone receptor (hTSHR-I, LGR3)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

levothyroxine sodium 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Endocrine disordersHypothyroidism✓ Approved

相关研究文献

PubMedCells2026-10-26

Can Thyroid Dysfunction Contribute to Infertility via Lipid Abnormalities?

Kelly Rose B RB, Hassoun Aya A AA, Stępniak Jan J, Kaczmarek Piotr P et al.

Thyroid dysfunction alters lipid metabolism and may impair reproduction, raising the possibility that lipid abnormalities contribute to thyroid-related infertility. This review evaluates dyslipidemia as a potential mechanistic link between these conditions. Thyroid hormones regulate hepatic LDL clearance, triglyceride-rich lipoprotein metabolism and HDL remodeling. Overt hypothyroidism commonly increases total and LDL cholesterol, changes that are partly reversible with levothyroxine, whereas lipid abnormalities in subclinical and central hypothyroidism are smaller and less consistent; hyperthyroidism generally lowers total and LDL cholesterol. Independently, adverse circulating lipid profiles are associated with reduced natural fecundability and poorer outcomes in selected assisted-reproduction studies. Experimental evidence identifies biologically coherent pathways involving ovarian steroidogenesis, follicular HDL function, oocyte cholesterol efflux and membrane signaling, endometrial receptivity and sperm membrane integrity. Human evidence supports both the thyroid-lipid and lipid-fertility relationships, but does not establish that lipid abnormalities mediate thyroid-related infertility. Interpretation is complicated by direct thyroid hormone effects, thyroid autoimmunity and metabolic confounding. Taken together, current findings support dyslipidemia as a biologically plausible potential contributor to thyroid-related reproductive dysfunction. Clinically, they suggest considering integrated assessment of thyroid and lipid status in reproductive-age adults and reassessment of the lipid profile after restoration of euthyroidism. Prospective preconception studies incorporating functional lipid measurements and formal mediation analyses are needed.

PMID 42929820
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PubMedCardiology in the young2026-10-26

Maternal thyroid disorders and risk of fetal CHD: a systematic review and meta-analysis.

Mangkuliguna Ghea G, Adrianto Nicholas N, Handisurya I Wayan Andrew IWA, Sibarani Candra Novi Ricardo CNR

To evaluate whether thyroid disorders during pregnancy correlate with the risk of CHD. Literature search was conducted across multiple databases, including PubMed/MedLine, Scopus, Cochrane Library, and grey literature repositories. Meta-analysis using a random-effect model was conducted. Newcastle-Ottawa Scale was used to determine the quality of studies. Grading of Recommendations, Assessment, Development, and Evaluations was used to evaluate the confidence in cumulative evidence. The study protocol was registered with the International Prospective Register of Systematic Reviews (CRD42024545867). A total of eight studies were included in the analysis. Maternal thyroid disorders were associated with the risk of CHDs (odd ratio 1.30, 95% confidence interval 1.07 to 1.57, P = 0.008). When categorised to specific subtypes, pooled studies reporting maternal hypothyroidism showed higher risk of developing CHD, even though it did not reach statistical significance (odds ratio 3.02, 95% confidence interval 0.57 to 16.05, P = 0.20). Exposure to maternal use of anti-thyroid drugs (odds ratio 4.44, 95% confidence interval 2.25 to 8.77, P < 0.0001) and levothyroxine (odds ratio 1.22, 95% confidence interval 1.08 to 1.37, P = 0.001) appeared to significantly increase the risk of CHD. All studies were judged to have good quality. The evidence generated from this study ranges from very low-to-low. Maternal thyroid disorders and exposure to thyroid-related medications appear to be associated with an elevated risk of CHD in fetuses.

PMID 42928471
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PubMedPhysical chemistry chemical physics : PCCP2026-10-26

Sodium alginate-stabilized gold nanoparticles synthesized via solution plasma sputtering for turn-on fluorescent detection of mercury(II) ions in water.

Chantaramethakul Jidapa J, Panomsuwan Gasidit G

Sodium alginate-stabilized AuNPs synthesized via solution plasma sputtering were coupled with Rhodamine 6G to construct a turn-on fluorescent sensor for mercury(II) ion detection in water. The probe exhibited a low detection limit of 0.022 µM, excellent selectivity, and good applicability to real water samples.

PMID 42929384
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PubMedNanoscale2026-10-26

Recent advances in structural and interfacial chemistry of Prussian blue analogues for sodium-ion batteries.

Jang Seunghye S, Kim Yuseul Y, Jo Changshin C

Prussian blue analogues (PBAs) have emerged as leading cathode materials for sodium-ion batteries owing to their open framework structure, low cost, and scalable synthesis. While early studies primarily focused on compositional and morphological optimization, recent advances have revealed that structural chemistry and interfacial reactions critically govern electrochemical performance, degradation behavior, and long-term stability. This mini review will highlight recent progress in understanding crystal water, structural evolution, surface degradation mechanisms, and emerging stabilization strategies. Particular attention will be given to the interplay between bulk structural characteristics and interfacial chemistry, which collectively determines the practical performance of PBA cathodes. By integrating these recent developments, we aim to provide a timely perspective on key challenges and future directions for the practical deployment of PBA cathodes in sodium-ion batteries.

PMID 42929254
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PubMedCardiovascular toxicology2026-10-26

The Pesticide Pyrethroid Metabolite 3-Phenoxybenzoic Acid (3-PBA) Impairs Human Cardiac Nav1.5 and Action Potential Depolarization.

de Lima Conceição Michael Ramon MR, Marques Leisiane Pereira LP, da Silva Alcantara Fabiana F, de Morais Rafael Leite Tavares RLT et al.

Pyrethroid insecticides (PYRs) are widely used worldwide, and their primary metabolite, 3-phenoxybenzoic acid (3-PBA), serves as a near-ubiquitous biomarker of human exposure to PYRs. While epidemiological data consistently link urinary 3-PBA to increased cardiometabolic risk and coronary heart disease, the underlying electrophysiological mechanisms of its direct potential cardiotoxicity remain unexplored. Parent PYRs are known to exert cardiotoxic effects by enhancing the late sodium current (INa-L) and inducing arrhythmia, but the direct effect of 3-PBA on heart excitability has not been previously investigated. This study demonstrates that 3-PBA interacts with human cardiac Nav1.5 expressed in Human Embryonic Kidney (HEK293) cells, and significantly increases INa-L in a concentration-dependent manner with an EC50 of 51.3 ± 5.1 µM. The metabolite does not alter the voltage dependence of activation and inactivation, but it significantly delays the recovery from inactivation of the peak sodium current. In human induced pluripotent stem cell-derived cardiomyocytes (CM-hiPSCs) and adult rat ventricular myocytes, 3-PBA reduced maximal depolarization rate (dV/dt), indicating impaired depolarization dynamics and reduced peak sodium current. At the organ level, acute exposure in isolated rat hearts did not significantly alter standard ECG parameters. Collectively, these findings suggest that 3-PBA is not electrophysiologically inert but directly modulates cardiac sodium channel function, although at supraphysiological concentration. This provides new evidence of the biological activity of 3-PBA and suggests that its cardiotoxic potential may become clinically relevant under conditions of high dose and chronic exposure or in susceptible populations.

PMID 42928408
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PubMedSurgical case reports2026-10-26

Life-Saving Emergency Decompression via a Clamshell Approach for Cardiac Arrest Caused by Hemorrhage of a Giant Mediastinal Ectopic Thyroid: A Case Report.

Ono Minori M, Watanabe Yui Y, Togo Takeo T, Nakano Yusuke Y et al.

Mediastinal ectopic thyroid tissue is rare and is usually asymptomatic. Intratumoral hemorrhage causing acute mediastinal compression and cardiac arrest is extremely uncommon. We report a case of cardiac arrest caused by hemorrhage of a giant mediastinal ectopic thyroid, successfully managed with venoarterial extracorporeal membrane oxygenation (VA-ECMO) and emergency surgical decompression by tumor removal. A 71-year-old woman with a long-standing anterior mediastinal tumor was transferred to our hospital because of dyspnea and shock after a fall. Contrast-enhanced CT revealed a giant anterior mediastinal tumor occupying the left hemithorax, with active extravasation and marked mediastinal deviation. Transarterial embolization was performed; however, she developed cardiac arrest shortly after embolization, presumably due to rapid tumor enlargement and severe mediastinal compression caused by intratumoral hemorrhage. Cardiopulmonary resuscitation was immediately initiated, and VA-ECMO was established. Emergency tumor removal and hemostasis were performed through a 4th-intercostal clamshell incision. The tumor occupied almost the entire left thoracic cavity and was extensively adherent to the chest wall and mediastinum, with particularly firm adhesion to the left brachiocephalic vein. The tumor was removed with combined resection of the left brachiocephalic vein. Histopathological examination revealed benign ectopic thyroid tissue without malignant findings. The postoperative course was complicated by bleeding, infection, acute kidney injury, and prolonged impaired consciousness. Postoperative hypothyroidism was identified after pathological confirmation of ectopic thyroid tissue, and levothyroxine replacement was initiated. The patient was transferred to a rehabilitation hospital on POD 72 and is currently living at home 1 year after surgery. Giant mediastinal ectopic thyroid tissue can cause fatal circulatory collapse when complicated by intratumoral hemorrhage. Although the patient was in a critical condition, she was successfully rescued by VA-ECMO followed by emergency decompression through surgical tumor removal.

PMID 42928950
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