| Size | Price | Stock | Qty |
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Purity: =98.11%
3,3',5'-Triiodo-L-thyronine (Reverse T3) is a thyroid hormone obtained by deiodination of the prohormone thyroxine. Reverse T3 inhibits the increase of sodium current generated by other thyroid hormone analogs in neonatal rat myocytes.
| ln Vitro |
T3 pre-treatment (0.1 mg/kg, administered intraperitoneally 2 h prior to brain death induction) reduced hepatic Bax gene expression and decreased cleaved Caspase-3 activation in the liver of brain-dead rats, indicating anti-apoptotic effects. [2]
- T3 pre-treatment did not alter the expression of inflammatory genes (IL-6, MCP-1, IL-1β) in the liver of brain-dead rats compared to vehicle-treated animals. [2] - T3 pre-treatment did not affect the expression of pro-mitotic markers (Cyclin-D and Ki-67) in the liver of brain-dead rats. [2] - T3 pre-treatment significantly reduced HO-1 protein levels (oxidative stress marker) in the liver of brain-dead rats. [2] - T3 pre-treatment significantly lowered STAT3 and Nrf2 gene expression in the liver of brain-dead rats. [2] |
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| ln Vivo |
T3 pre-treatment (0.1 mg/kg, intraperitoneal injection 2 h before brain death induction) significantly reduced plasma levels of AST and ALT in brain-dead rats, indicating attenuated hepatic injury. [2]
- T3 pre-treatment did not significantly reduce the amount of vasoactive agents (HAES or noradrenaline) needed to maintain mean arterial pressure above 80 mmHg in brain-dead rats. [2] - T3 pre-treatment significantly reduced the number of cleaved Caspase-3 positive cells in the liver of brain-dead rats, confirming reduced apoptosis. [2] - T3 pre-treatment did not affect the number of Ki-67 positive proliferating cells in the liver of brain-dead rats. [2] - T3 pre-treatment significantly reduced HO-1 total intensity per area in the liver of brain-dead rats, indicating reduced oxidative stress. [2] |
| Cell Assay |
RNA isolation and real-time PCR: Total RNA was isolated from whole liver sections using TRIzol. cDNA was synthesized using oligo-dT and M-MLV reverse transcriptase. Real-time PCR was performed using SYBR Green mastermix. Gene expression of Bax, Bcl-2, IL-6, IL-1β, MCP-1, Cyclin-D, STAT3, and Nrf2 was analyzed. Expression was normalized to β-actin mRNA content. Results were expressed as 2^(-ΔΔCT). All samples were analyzed in triplicate. [2]
- Immunohistochemistry (cleaved Caspase-3, Ki-67, HO-1): Paraffin-embedded liver sections (3 μm) were deparaffinized and subjected to heat-induced antigen retrieval using EDTA buffer (pH 8.0) for cC3, citrate buffer (pH 6.0) for Ki-67, or Tris/HCl buffer (pH 9.0) for HO-1. Sections were stained with primary antibodies against cC3, Ki-67, or HO-1 using an indirect immunoperoxidase technique. Endogenous peroxidase was blocked with H2O2. Horseradish peroxidase-conjugated secondary and tertiary antibodies were used. The reaction was developed using DAB and H2O2. Sections were counterstained with Mayer hematoxylin. Positive cells per field were counted by two blinded researchers in 10 microscopic fields at 20x magnification. HO-1 intensity quantification was performed using Aperio Image Scope with positive pixel count v9, presented as total intensity per area (mm²). [2] - Histopathological evaluation (H&E staining): Liver sections (3 μm) were stained with hematoxylin-eosin and blindly scored by a pathologist for conservation of cytoarchitecture, lobule organization, hepatocyte appearance, localization of portal and central veins, and amount of necrosis. [2] |
| Animal Protocol |
Brain death model and T3 treatment: Male Fisher F344 rats (250-300 g) were anesthetized with isoflurane and mechanically ventilated. Brain death was induced by slow inflation (0.16 ml/min) of a Fogarty catheter placed in the epidural space until a steep rise in mean arterial pressure was noted. Brain death was confirmed by absence of corneal reflexes and a positive apnea test. T3 (0.1 mg/kg) or vehicle (0.1 N NaOH, pH 7.4) was administered intraperitoneally 2 hours before brain death induction. After 4 hours of brain death, blood and liver tissue were collected. Sham-operated rats were ventilated for 0.5 h under anesthesia. n=7 per group. [2]
- Hemodynamic management: Mean arterial pressure was maintained above 80 mmHg using colloid infusion (polyhydroxyethyl starch 10%, maximum rate 1 ml/h) and, if unresponsive, intravenous noradrenaline drip (1 mg/ml). A homeothermic blanket control system was used. [2] |
| References |
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| Additional Infomation |
3,3',5'-Triiodo-L-thyroxine is a 3,3',5'-triiodothyroxine. It is the zwitterion tautomer of 3,3',5'-triiodo-L-thyroxine. It is a metabolite of thyroxine, formed by a peripheral enzymatic deiodination reaction of T4 at the 5-position of the inner ring of the iodothyroxine nucleus. See also: Iodothyroxine (note moved to).
In brain-dead rats, plasma levels of free T3 fall to 50% of baseline within 1 hour and become undetectable after 9 hours. [2] - T3 pre-conditioning has been shown to exert anti-apoptotic and pro-mitotic effects in liver tissue following ischemia/reperfusion injury. The present study demonstrates for the first time anti-apoptotic effects of T3 pre-conditioning in the brain death setting. [2] - The mechanism by which T3 exerts its anti-apoptotic effects remains intact in brain-dead donors and is achieved in a short time frame (2 hours pre-treatment). [2] - T3 pre-treatment reduced apoptosis at the transcriptional level (Bax) and at the execution phase (cleaved Caspase-3). [2] - Despite reduced apoptosis, T3 therapy did not alter cell cycle regulation (Cyclin-D) or proliferation (Ki-67) in this model. [2] |
| Molecular Formula |
C15H12I3NO4
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|---|---|
| Molecular Weight |
650.9735
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| Exact Mass |
650.79
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| CAS # |
5817-39-0
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| Related CAS # |
Reverse T3-13C6 hydrochloride;1217676-14-6
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| PubChem CID |
644280
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| Appearance |
Off-white to yellow solid powder
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| Density |
2.4±0.1 g/cm3
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| Boiling Point |
534.6±50.0 °C at 760 mmHg
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| Melting Point |
234-238ºC(lit.)
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| Flash Point |
277.1±30.1 °C
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| Vapour Pressure |
0.0±1.5 mmHg at 25°C
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| Index of Refraction |
1.763
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| LogP |
5.39
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
5
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| Rotatable Bond Count |
5
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| Heavy Atom Count |
23
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| Complexity |
402
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| Defined Atom Stereocenter Count |
1
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| SMILES |
C1=CC(=C(C=C1C[C@@H](C(=O)O)N)I)OC2=CC(=C(C(=C2)I)O)I
|
| InChi Key |
HZCBWYNLGPIQRK-LBPRGKRZSA-N
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| InChi Code |
InChI=1S/C15H12I3NO4/c16-9-3-7(4-12(19)15(21)22)1-2-13(9)23-8-5-10(17)14(20)11(18)6-8/h1-3,5-6,12,20H,4,19H2,(H,21,22)/t12-/m0/s1
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| Chemical Name |
(2S)-2-amino-3-[4-(4-hydroxy-3,5-diiodophenoxy)-3-iodophenyl]propanoic acid
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
H2O : ~3.57 mg/mL (~5.48 mM)
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|---|---|
| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.5362 mL | 7.6808 mL | 15.3617 mL | |
| 5 mM | 0.3072 mL | 1.5362 mL | 3.0723 mL | |
| 10 mM | 0.1536 mL | 0.7681 mL | 1.5362 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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