Liothyronine Sodium
(Synonyms: 三碘代甲状腺素钠盐) 目录号 : GC12409
Liothyronine sodium 是一种强效的甲状腺激素受体TRα和TRβ激动剂，其 Ki 值为 2.33nM。
Cas No.:55-06-1
Sample solution is provided at 25 µL, 10mM.
;)
_1-7.$$$37316672@70.jpg');)
;)
;)
_273-287.$$$36806353@46.jpg');)
_1-16.$$$37156877@44.jpg');)
;)
;)
;)
_1124-1138.$$$35908550@30.jpg');)
_766-780.$$$37100057@30.jpg');)
_418-432.$$$36893736@30.jpg');)
_240-255.$$$35108512@29.jpg');)
_533-545.$$$36543525@28.jpg');)
_264-276.$$$36600053@22.jpg');)
_2214998.$$$@0.jpg');)
Liothyronine sodium is a potent thyroid hormone receptor TRα and TRβ agonist with Ki values of 2.33nM[1]. Liothyronine sodium is an active form of thyroid hormone that is chemically almost identical to the endogenous thyroid hormone triiodothyronine (T3)[2]. Liothyronine sodium is usually used in the replacement treatment of hypothyroidism[3], and can also be used in the treatment of thyroid cancer and the detection of thyroid function[4]. In addition, Liothyronine sodium is also used in the study of other metabolic related diseases, such as obesity[5].
In vitro, Liothyronine sodium(100µM) treatment of Jurkat hTIGIT cells and CHOK1-hPVR cells for 48h reversed the IL-2 secretion inhibition resulted by TIGIT/PVR ligation without affecting cell viability[6]. Liothyronine sodium(100nM) stimulates the proliferation of hepatocellular carcinoma cells overexpressing TRβ1[1].
In vivo, Liothyronine sodium(25μg/kg; 1h post-tMCAO; intravenously) reduced infarct volumes in a dose-dependent manner, with reduced efficacy at 4.5h post-tMCAO(P = 0.066) and no effect at 8h post-tMCAO(P > 0.999), while demonstrating a persistent protective effect for 72h post-tMCAO (P < 0.01) and accelerating motor function recovery by day 3 (P < 0.05), accompanied by reduced cerebral edema, diminished blood–brain barrier leakage, and decreased aquaporin-4 expression in stroke mice[7].
References:
[1] Lin, K. H., Lin, Y. W., Parkison, C., & Cheng, S. Y. (1994). Stimulation of proliferation by 3,3',5-triiodo-L-thyronine in poorly differentiated human hepatocarcinoma cells overexpressing beta 1 thyroid hormone receptor. Cancer letters, 85(2), 189–194.
[2] MORTON J. H. (1957). Sodium liothyronine in metabolic insufficiency syndrome and associated disorders; preliminary report. Journal of the American Medical Association, 165(2), 124–129.
[3] Escobar-Morreale, H. F., Botella-Carretero, J. I., & Morreale de Escobar, G. (2015). Treatment of hypothyroidism with levothyroxine or a combination of levothyroxine plus L-triiodothyronine. Best practice & research. Clinical endocrinology & metabolism, 29(1), 57–75.
[4] Salas-Lucia, F., & Bianco, A. C. (2022). T3 levels and thyroid hormone signaling. Frontiers in endocrinology, 13, 1044691.
[5] Krotkiewski M. (2000). Thyroid hormones and treatment of obesity. International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity, 24 Suppl 2, S116–S119.
[6] Zhou, X., Du, J., Wang, H., Chen, C., Jiao, L., Cheng, X., Zhou, X., Chen, S., Gou, S., Zhao, W., Zhai, W., Chen, J., & Gao, Y. (2020). Repositioning liothyronine for cancer immunotherapy by blocking the interaction of immune checkpoint TIGIT/PVR. Cell communication and signaling : CCS, 18(1), 142.
[7] Ullrich, D., Führer, D., Heuer, H., Mayerl, S., Haupeltshofer, S., Schmitt, L. I., Leo, M., Szepanowski, R. D., Hagenacker, T., Schwaninger, M., Kleinschnitz, C., & Langhauser, F. (2025). Triiodothyronine treatment in mice improves stroke outcome and reduces blood-brain barrier damage. European thyroid journal, 14(1), e240143.
Liothyronine sodium是一种强效的甲状腺激素受体TRα和TRβ激动剂，其Ki值为 2.33nM[1]。Liothyronine sodium是一种活性形式的甲状腺激素，其化学性质几乎与内源性甲状腺激素三碘甲状腺原氨酸（T3）相同[2]。Liothyronine sodium通常用于甲状腺功能减退症的替代治疗[3]，也可用于甲状腺癌的治疗和甲状腺功能的检测[4]。此外，Liothyronine sodium还用于其他与代谢相关的疾病研究，如肥胖[5]。
在体外实验中，用100µM的Liothyronine sodium 处理Jurkat hTIGIT细胞和CHOK1-hPVR细胞 48小时，可逆转TIGIT/PVR结合导致的IL-2分泌抑制，且不影响细胞活力[6]。100nM的Liothyronine sodium可刺激过表达 TRβ1 的肝癌细胞增殖[1]。
在体内实验中，在中风小鼠模型中，Liothyronine sodium(25μg/kg；短暂性大脑中动脉闭塞（tMCAO）后1小时；静脉注射）以剂量依赖性方式减少梗死体积，在术后4.5小时给药时效性降低（P = 0.066），在 术后8小时给药则无效（P > 0.999），且在tMCAO后 72小时内显示出持续的保护效果（P < 0.01），并在第3天加速运动功能恢复（P < 0.05），同时观察到脑水肿减轻、血脑屏障渗漏减少以及水通道蛋白-4 表达降低[7]。
| Cell experiment [1]: | |
Cell lines | Jurkat-hTIGIT and CHOK1-hPVR cells |
Preparation Method | CHOK1-hPVR were seeded into 24- well plates at a density of 1 × 105 cells/well and allowed for cell adhesion. Jurkat-hTIGIT were added into the plates pre-cultured with CHOK1-hPVR at a density of 2 × 105 cells/well with the effector: target ratio of 2:1. Jurkat-hTIGIT cells were stimulated with the anti-human CD3 (1μg/mL) and anti-human CD28 (0.5μg/mL). Liothyronine sodium(100μM) were added in the coculture system, and a functional anti-TIGIT antibody served as the positive control. After 44h of coculture, the protein transport inhibitor was added and incubated for another 4h. Then the cells were harvested, washed, and followed by fixation and permeabilization. Afterwards, the permeabilized JurkathTIGIT cells were stained with anti-human IL-2 APC or isotype control antibody for 30min at 4°C. |
Reaction Conditions | 100μM; 48h |
Applications | Liothyronine sodium could reverse the IL-2 secretion inhibition resulted by TIGIT/PVR ligation without affecting the proliferation of tumor cells. |
| Animal experiment [2]: | |
Animal models | C57BL/6N mice |
Preparation Method | Mice received Liothyronine sodium at doses of either 10, 25, or 50μg/kg bw. Stock solution (10mg/ml in 1 M HCl:EtOH (1:4)) was diluted in 0.9% NaCl and intravenously injected via the tail vein, either 1h prior to tMCAO induction or 1, 4.5, or 8h after tMCAO induction. As control, mice received equivalent volumes of 0.9% NaCl. Functional assessment was conducted 24 or 72h post tMCAO. Mice were sacrificed 24 or 72h after tMCAO and brains were removed for Western blot or histological analysis. |
Dosage form | 10, 25, or 50μg/kg; 24 or 72h; intravenously injected via the tail vein |
Applications | Liothyronine sodium (25μg/kg, 1h post-tMCAO, intravenously) reduced infarct volumes in a dose-dependent manner, with reduced efficacy at 4.5h post-tMCAO(P = 0.066) and no effect at 8h post-tMCAO(P > 0.999), while demonstrating a persistent protective effect for 72h post-tMCAO (P < 0.01) and accelerating motor function recovery by day 3 (P < 0.05), accompanied by reduced cerebral edema, diminished blood–brain barrier leakage, and decreased aquaporin-4 expression in stroke mice. |
References: | |
| Cas No. | 55-06-1 | SDF | |
| 别名 | 三碘代甲状腺素钠盐 | ||
| 化学名 | sodium;(2S)-2-amino-3-[4-(4-hydroxy-3-iodophenoxy)-3,5-diiodophenyl]propanoate | ||
| Canonical SMILES | C1=CC(=C(C=C1OC2=C(C=C(C=C2I)CC(C(=O)[O-])N)I)I)O.[Na+] | ||
| 分子式 | C15H12I3NO4.Na | 分子量 | 672.96 |
| 溶解度 | ≥ 23.47 mg/mL in DMSO with ultrasonic and warming | 储存条件 | Store at -20°C,protect from light |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 1.486 mL | 7.4299 mL | 14.8597 mL |
| 5 mM | 0.2972 mL | 1.486 mL | 2.9719 mL |
| 10 mM | 0.1486 mL | 0.743 mL | 1.486 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet