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T2 Powder, L-Triiodothyronine, Triiodothyronine manufacturer / supplier in China, offering Pharmaceutical Amino Acid 3, 5-Diiodo-L-Thyronine T2 Powder CAS 1041-01-6, Top Quality Safe Delivery Methenolone Enanthate Primobolan Depot, 99% Purity and Best Price Steroid Raw Powder 4-Chlorotestosterone and so on.

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Pharmaceutical Amino Acid 3, 5-Diiodo-L-Thyronine T2 Powder CAS 1041-01-6

FOB Price: US $1 / g
Min. Order: 10 g
Min. Order FOB Price
10 g US $1/ g
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Port: Shanghai, China
Production Capacity: 2000kg/M
Payment Terms: T/T, Western Union, Money Gram, bitcoin

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Basic Info
  • Model NO.: 1041-01-6
  • Customized: Non-Customized
  • Suitable for: Elderly, Adult
  • Purity: >99%
  • CAS No: 1041-01-6
  • MW: 650.97
  • Delivery Method: Express, Air, Sea (Optional)
  • Trademark: WHSO
  • Specification: 1g, 10g, 100g, 1kg, 5kg, 25kg, etc
  • HS Code: 2942000000
  • Powder: Yes
  • Certification: GMP, ISO 9001, USP, BP
  • State: Solid
  • Appearance: White Powder
  • Mf: C15h12I3no4
  • Delivery Date: 1-7 Days
  • Name: L-Triiodothyronine T3 Powder
  • Transport Package: as You Requiry/Discreet Packing
  • Origin: China
Product Description
CAS 55-06-1 T3 L-Triiodothyronine Raw Steroid White to Beige Powder
Quick Details:

Synonyms:L-Triiodothyronine;T3;T3 Na;3,3',5-Triiodo-L-thyronine;L-triiodothyronine sodium;Liothyronine Sodium;
CAS: 55-06-1 
Assay: 99.2%(HPLC)
Apprarance:White to beige powder 
Usage:Weight Training and Fat Burners,T3 (Cytomel) is a thyroid hormone drug fairly commonly used for fat loss, particularly in the context of anabolic steroid cycles. T3 is naturally produced in the body as a result of T4 (thyroxine) production by the thyroid. Oral administration of T3 can yield higher levels of serum T3 than would occur naturally, allowing faster fat loss and in some cases potentially greater GH production an greater anabolism.


L-triiodothyronine (T3) has previously been shown to substance fast-phase, depolarization-induced 45Ca uptake and [3H-gamma-aminobutyric acid release by rat brain synaptosomes at low nanomolar concentrations comparable to those reported for whole brain. Neverthless, the physiologic importance of these nonnuclear-mediated effects of T3 has remained uncertain, a part because specific mechanisms and the presence of T3 at pesumptive sites of action have not been demonstrated. Isotopic studies showing that L-tetraiodothyronine thyroxine, T4) and T3 are concentrated in synaptosomes, and that T4 is deiodinated to T3 suggested that endogenous levels of T3 in nerve terminals are probably much higher than in other compartments of the brain. In the present study we confirmed that endogenous levels of T3 in nerve terminals are at least eightfold higher, and may be as much as 60-fold higher, than in whole brain. More importantly, we showed that both 125I-labeled T3 and endogenous T3, but not 125I-T4 or endogenous T4, are released from depolarized synaptosomes, primarily by a Ca2+-dependent process. This demonstrates a mechanism for raising the level of T3 within the synapse, where the hormone may interact with pre- and postsynaptic binding (or uptake) sites, and suggests that the peripheral hormone T3 may be a neurotransmitter.


Because T3 has a short half-life, divided doses are preferable to a single dose, except where total daily dosing is small. For example, with a dosing of 12.5 this would best be taken as a single dose in the morning, but with 50 mcg/day, dividing the daily amount into three or four doses would be better than taking the entire amount at one time.
After extended use of T3 at a suppressive dose, natural production is suppressed for some time after discontinuing T3 use. Generally the duration appears related to the length of use. In cases of brief usage there's typically no noticeable period of low function post-cycle, but with extended cycles the duration of low function can be measured for as long as about six weeks in some cases. The literature article "Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy" provides an example of difficulty that can be encountered in recovering good thyroid production after a long period of oral thyroid use. While in this study all the subjects did recover "normal" thyroid production, as also happens routinely in bodybuilding use, the "normal" that they ended up with was the rock-bottom end of the normal range, about 40 mcg/dL total serum T4 and about 80 ng/dL total serum T3. These are not levels one wants to be at, and are low enough that metabolism would be impaired.
High dosage of T3, typically starting at about 75 mcg/day but in some cases not starting until about 100 mcg/day, can cause tachycardia (elevated heart rate) and muscle weakness, and can be catabolic or at the least reduce anabolism. High dose anabolic steroids, of course, tend to mask this latter effect. Very high levels of T3 are dangerous to the heart.
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