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D-Thyroxine Sale

(Synonyms: D-甲状腺素; D-T4) 目录号 : GC66682

D-Thyroxine (D-T4) 是一种甲状腺激素,可以抑制 TSH 的分泌。D-Thyroxine 可用于高胆固醇血症的研究。

D-Thyroxine Chemical Structure

Cas No.:51-49-0

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产品描述

D-Thyroxine (D-T4) is a thyroid hormone that can inhibit TSH secretion. D-Thyroxine can be used for the research of hypercholesterolemia[1][2].

[1]. Bantle JP, et, al. Comparison of effectiveness of thyrotropin-suppressive doses of D- and L-thyroxine in treatment of hypercholesterolemia. Am J Med. 1984 Sep;77(3):475-81.
[2]. Gless KH, et, al. Influence of D-thyroxine on plasma thyroid hormone levels and TSH secretion. Horm Metab Res. 1977 Jan;9(1):69-73.

Chemical Properties

Cas No. 51-49-0 SDF Download SDF
别名 D-甲状腺素; D-T4
分子式 C15H11I4NO4 分子量 776.87
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1 mM 1.2872 mL 6.4361 mL 12.8722 mL
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Research Update

D-Thyroxine reduces lipoprotein(a) serum concentration in dialysis patients

J Am Soc Nephrol 1998 Jan;9(1):90-6.PMID:9440092DOI:10.1681/ASN.V9190.

Uremia raises lipoprotein(a) (Lp(a)) serum concentration and the risk of arteriosclerosis in dialysis patients. The treatment of high Lp(a) levels is not satisfactory today. The decrease of Lp(a) in hypothyroid patients on L-T4 therapy raised the question of whether dextro-thyroxine (D-Thyroxine) reduces not only serum cholesterol, but also Lp(a) serum concentration. In a single-blind placebo-controlled study, the influence of D-Thyroxine therapy on Lp(a) serum concentration was evaluated in 30 hemodialysis patients with elevated Lp(a) serum levels. Lp(a) was quantified in parallel by two methods, i.e., rocket immunoelectrophoresis and nephelometry, and apo(a) isoforms were determined by a sensitive immunoblotting technique. Regardless of the apo(a) isoforms, 6 mg/d D-Thyroxine reduced elevated Lp(a) levels significantly by 27 +/- 13% in 20 dialysis patients (P < 0.001) compared with 10 control subjects (-9.9 +/- 8.4%). In parallel, D-Thyroxine therapy significantly lowered total cholesterol (P < 0.001), LDL cholesterol (P < 0.001), and LDL cholesterol/HDL cholesterol ratio (P < 0.01); raised T4 and T3 serum levels; and suppressed thyroid-stimulating hormone secretion without causing clinical symptoms of hyperthyroidism in any of the patients. D-Thyroxine reduces elevated serum Lp(a) concentration in dialysis patients. The effect in nondialysis patients can be expected but remains to be proven.

D-Thyroxine in hyperbetalipoproteinaemia

S Afr Med J 1975 Oct 4;49(42):1757-8.PMID:171778doi

D-Thyroxine was administered intermittently to 11 patients with hyperlipoproteinaemia (Fredrickson type lla). To avoid possible untoward cardiac stimulation, practolol was prescribed with it. Cholesterol levels were measured regularly over a period of 4 years. A temporary drop of about 15% in the mean cholesterol level was obtained. It is, however, concluded that the over-all response is unimpressive.

Comparison of effectiveness of thyrotropin-suppressive doses of D- and L-thyroxine in treatment of hypercholesterolemia

Am J Med 1984 Sep;77(3):475-81.PMID:6475988DOI:10.1016/0002-9343(84)90107-4.

In an attempt to compare the cholesterol-lowering effects of equivalent doses of D- and L-thyroxine, 10 euthyroid, hypercholesterolemic subjects were treated with graded doses of each medication in a cross-over design using thyrotropin suppression following thyrotropin-releasing hormone administration as the end-point. The mean thyrotropin-suppressive dose of D-Thyroxine was 2.4 +/- 0.66 mg per day, which resulted in mean reductions of 10 percent in total plasma cholesterol, 10 percent in plasma low-density lipoprotein cholesterol, and 11 percent in plasma high-density lipoprotein cholesterol. The mean thyrotropin-suppressive dose of L-thyroxine was 135 +/- 46 micrograms per day, which resulted in mean reductions of 7 percent in total plasma cholesterol, 6 percent in plasma low-density lipoprotein cholesterol, and 14 percent in plasma high-density lipoprotein cholesterol. The reductions in total, low-density, and high-density cholesterol achieved with D-Thyroxine were not significantly different from those achieved with L-thyroxine. Neither medication produced a significant increase in heart rate or ventricular ectopy as determined by Holter monitoring. These data do not support the belief that D-Thyroxine has a preferential cholesterol-lowering effect in humans when compared with equivalent doses of L-thyroxine. In addition, both D- and L-thyroxine reduced plasma high-density lipoprotein cholesterol.

Enatioselective quantitative separation of D- and L-thyroxine by molecularly imprinted micro-solid phase extraction silver fiber coupled with complementary molecularly imprinted polymer-sensor

J Chromatogr A 2010 Jun 25;1217(26):4255-66.PMID:20483419DOI:10.1016/j.chroma.2010.04.055.

Thyroxine is a known disease biomarker which demands a highly sensitive and selective technique to measure ultratrace level with enantiodifferentiation of its optical isomers (d- and l-), in real samples. In this work, an approach of hyphenation between molecularly imprinted micro-solid phase extraction and a complementary molecularly imprinted polymer-sensor was adopted for enantioseparation, preconcentration, and analysis of d- and l-thyroxine. In both techniques, the same imprinted polymer, coated on a vinyl functionalized self-assembled monolayer modified silver wire, was used as the respective extraction fiber as well as sensor material. This combination enabled enhanced preconcentration of test analyte substantially so as to achieve the stringent limit [limit of detection: 0.0084 ng mL(-1), RSD=0.81%, S/N=3 (D-Thyroxine); 0.0087 ng mL(-1), RSD=0.63%, S/N=3 (l-thyroxine)] of clinical detection of thyroid-related diseases, without any problems of non-specific false-positive contribution and cross-reactivity.

Influence of D-Thyroxine on plasma thyroid hormone levels and TSH secretion

Horm Metab Res 1977 Jan;9(1):69-73.PMID:403117DOI:10.1055/s-0028-1093587.

Triiodothyronine (T3), thyroxine (T4), basal TSH and TSH after stimulation with TRH were determined in healthy subjects and patients treated with D-Thyroxine (DT4). After a dosage of 6 mg DT4 the D/L T4 plasma concentration rose about 4-fold 4 hours after application and was only moderately elevated 14 hours later. To achieve constantly elevated T4 levels 3 mg DT4 were applied in the further experiment every 12 hours. The D/L T4 plasma concentration rose 2.5-4-fold and there was a small but significant increase of the D/L T3 plasma concentration. 74 hours after onset of treatment basal TSH was below detectable limits and the increase of TSH 30 min after injection of 200 mug TRH (TRH test) was only about 15% compared to zero time. The time course of TSH suppression was investigated after treatment with DT4 and LT4 (single dosage of 3 mg). TRH-tests were performed before, 10, 26, 50 and 74 hours after the first dosage of D or LT4. There was no difference in the time course of basal TSH and TSH stimulated by TRH. In 10 patients on DT4 long-term therapy, basal and stimulated TSH were found to be below the detectable limits of 0.4 mug/ml. Our results show that (1) plasma half-life of DT4 is less than 1 day, (2) TSH suppression after D and LT4 treatment is very similar, and (3) in patients on long-term DT4 treatment, TSH plasma concentration is below detectable limits even after stimulation with TRH.