3,3'-t2

[michael3435]

What is 3,3’ Diiodo-L-Thyronine?
Also known as 3,3’-T2, this is a naturally occurring metabolite of thyroid hormone.

Where does T2 come from?
In order to explain this, a brief explanation of the basic endocrinology surrounding the thyroid must be explained:
A hormone called TSH (thyroid stimulating hormone) is released from the anterior pituitary gland in the brain. It binds to receptors on the thyroid gland and this is what signals for the production and release of thyroid hormones, T3 and T4. There are many biochemical reactions, which create different metabolites of these hormones. 3,3’-T2 is one of these naturally occurring metabolites, and actually turns out to be active, contrary to what was once believed.

What does 3,3’-T2 do?
Although not as potent and active as T3 (which is a prescription drug) or 3,5-T2, 3,3’-T2 has been shown to have some benefits. It increases liver oxidation consumption and, most notably, it has activity in brown adipose tissue independent of protein synthesis (1,2). This is very important because even though T3 has extensive fat burning effects, it also has detrimental actions in muscle. In fact, one study found that for every 3 pounds of fat lost with T3, 1 pound of muscle was lost as well (3). This does not appear to be the case with 3-3’-T2. In addition, studies have found that T2 does not suppress TSH enough to the point where the thyroid has any change in activity (4).
The research on the T2 metabolites is still in its infancy so there may be plenty of exciting benefits that this compound has that we are not aware of yet. Research on other thyroid hormone metabolites (such as 3,5-T2) has been very positive.


1. Lanni A, et al. "Calorigenic effect of diiodothyronines in the rat." J Physiol 1996 Aug 1;494 (Pt 3):831-7
2. Goglia F, et al. "Action of thyroid hormones at the cellular level: the mitochondrial target." FEBS Lett 1999 Jun 11;452(3):115-20
3. Lovejoy JC, et al. "A paradigm of experimentally induced mile hyperthyroidism: effects on nitrogen balance, body composition, and energy expenditure in healthy young men." J Clin Endocrinol Metab 1997 Mar;82(3):765-70
4. 3,5-Diiodo-L-thyronine (T2) has selective thyromimetic effects in vivo and in vitro. SG Ball, J Sokolov, and WW Chin. Journal of Molecular Endocrinology, Vol 19, Issue 2, 137-147

[BringnIt]

Don't rats have considerably more BAT than humans?

[michael3435]

Don't rats have considerably more BAT than humans?

i think so but i am not sure. it would depend on how old the human is we are talking about too.

[JornT]

It increases liver oxidation consumption and, most notably, it has activity in brown adipose tissue independent of protein synthesis (1,2). This is very important because even though T3 has extensive fat burning effects, it also has detrimental actions in muscle. In fact, one study found that for every 3 pounds of fat lost with T3, 1 pound of muscle was lost as well (3). This does not appear to be the case with 3-3’-T2.

The part that the effects of 3,3' happen independent of protein synthesis seem to come from this paper:

Acta Endocrinol (Copenh). 1992 Dec;127(6):542-6.

Studies on the rapid stimulation of mitochondrial respiration by thyroid hormones.
O'Reilly I, Murphy MP.

Injection of L-3,5-diiodothyronine (T2) into rats made hypothyroid by 6-n-propyl-2-thiouracil (PTU) increased the respiration rates of subsequently isolated liver mitochondria; this stimulation of respiration by T2 occurred in the presence of cycloheximide and is therefore independent of protein synthesis on cytoplasmic ribosomes. Injection of T3 into PTU-treated rats had a lesser effect than T2 on the respiration rates of subsequently isolated mitochondria; as PTU is an inhibitor of 5'-iodothyronine deiodinases, which convert T3 into T2 in vivo, the rapid stimulation of mitochondrial respiration by T3, which has been shown in a range of systems, may not be due directly to T3 itself, but may be mediated by its deiodination product T2. Injection of T2, or T3, into hypothyroid or euthyroid rats had no effect on the percentage activity of mitochondrial pyruvate hydrogenase assayed 30 min later. The amount of active pyruvate dehydrogenase is regulated by changes in mitochondrial calcium concentration and matrix ATP/ADP ratio; therefore these parameters are not persistently affected by treatment with T3 or T2. In addition, the total amount of pyruvate dehydrogenase present was the same in euthyroid and hypothyroid rats, indicating that the expression of this enzyme is not stringently controlled by thyroid hormone status.

I have not read the fulltext yet, but the way I read it is that the effects of 3,3' doen't require protein synthesis for it's effects (in contrast to T3)...not that 3,3' won't have a negative effect on protein synthesis.

[7percent]

So anything about doses? I'm thinking of running 3,3 for 4 weeks, I highly doubt w/e the negligible hit to protein synthesis will do anything. Amirite?

[michael3435]

So anything about doses? I'm thinking of running 3,3 for 4 weeks

damn, i forgot to include the doses. i knew i was forgetting something.

i would start out at 100 mcg up to 4 times a day. 3,5'-T2 is much more potent than 3,3'-T2 so you may want to look into combining them.

[michael3435]

The part that the effects of 3,3' happen independent of protein synthesis seem to come from this paper:

Acta Endocrinol (Copenh). 1992 Dec;127(6):542-6.

Studies on the rapid stimulation of mitochondrial respiration by thyroid hormones.
O'Reilly I, Murphy MP.

Injection of L-3,5-diiodothyronine (T2) into rats made hypothyroid by 6-n-propyl-2-thiouracil (PTU) increased the respiration rates of subsequently isolated liver mitochondria; this stimulation of respiration by T2 occurred in the presence of cycloheximide and is therefore independent of protein synthesis on cytoplasmic ribosomes. Injection of T3 into PTU-treated rats had a lesser effect than T2 on the respiration rates of subsequently isolated mitochondria; as PTU is an inhibitor of 5'-iodothyronine deiodinases, which convert T3 into T2 in vivo, the rapid stimulation of mitochondrial respiration by T3, which has been shown in a range of systems, may not be due directly to T3 itself, but may be mediated by its deiodination product T2. Injection of T2, or T3, into hypothyroid or euthyroid rats had no effect on the percentage activity of mitochondrial pyruvate hydrogenase assayed 30 min later. The amount of active pyruvate dehydrogenase is regulated by changes in mitochondrial calcium concentration and matrix ATP/ADP ratio; therefore these parameters are not persistently affected by treatment with T3 or T2. In addition, the total amount of pyruvate dehydrogenase present was the same in euthyroid and hypothyroid rats, indicating that the expression of this enzyme is not stringently controlled by thyroid hormone status.

I have not read the fulltext yet, but the way I read it is that the effects of 3,3' doen't require protein synthesis for it's effects (in contrast to T3)...not that 3,3' won't have a negative effect on protein synthesis.

thanks for posting this. you are correct that its effects are independent of protein synthesis. i think this becomes more important when we compare it to the effects of T3, which we now know are significantly different. to be honest i am not sure of the mechanism by which T3 affects protein synthesis. do you have any info on this?

btw, what you posted is talking about 3,5', NOT 3,3'.

I highly doubt w/e the negligible hit to protein synthesis will do anything. Amirite?

what do you mean? there shouldnt be any effect on protein synthesis from 3,3'-T2

[7percent]

thanks for posting this. you are correct that its effects are independent of protein synthesis. i think this becomes more important when we compare it to the effects of T3, which we now know are significantly different. to be honest i am not sure of the mechanism by which T3 affects protein synthesis. do you have any info on this?

btw, what you posted is talking about 3,5', NOT 3,3'.


what do you mean? there shouldnt be any effect on protein synthesis from 3,3'-T2

Oh the article above was 3,5.

[NO HYPE]

3,5'-T2 is much more potent than 3,3'-T2 so you may want to look into combining them.

On an additional note....

originally posted by NO HYPE
3,5-diiodo-L-thyronine and/or their metabolites [which retain the same key structure-activity characteristics] can suppress TSH levels to a degree which can lead to lethargy, fatigue, cognitive impairment, depression ect. (Joffe and Sokolov, 1994). Alternatively, utilizing a 3,3' diiodothyroacetic isomer, would minimize the aforementioned degree of TSH suppression and it's undesireable effects.

[michael3435]

On an additional note....

originally posted by NO HYPE
3,5-diiodo-L-thyronine and/or their metabolites [which retain the same key structure-activity characteristics] can suppress TSH levels to a degree which can lead to lethargy, fatigue, cognitive impairment, depression ect. (Joffe and Sokolov, 1994). Alternatively, utilizing a 3,3' diiodothyroacetic isomer, would minimize the aforementioned degree of TSH suppression and it's undesireable effects.

where did you get this info? source number 4 shows that neither metabolite causes any significant suppression of TSH. this might be different for thyroacetic acids.

[BringnIt]

I'm trying to recall all the thyroidal products I've tried, but I've never really had positive results from the ones I can think of (most recently Mitotropin, for certain). Based on the testimonials I get as well (through my work), thyroid analogues typically are poorly received.

Could this be a dosage issue?

[michael3435]

I'm trying to recall all the thyroidal products I've tried, but I've never really had positive results from the ones I can think of (most recently Mitotropin, for certain). Based on the testimonials I get as well (through my work), thyroid analogues typically are poorly received.

Could this be a dosage issue?

yes. other issues could be a lack of 3,5'-T2 which is more active than 3,3'-T2 to my understanding. my guess is that you simply did not notice the results. just because it is a thyroidal compound doesnt mean it will increase your metabolic rate and have the other expected benefits of T3. we see here that it has been shown to have activity in brown adipose tissue. i am willing to bet that if you were to measure body fat with a precise mechanism, you would have seen a decrease (given a caloric maintenance). the 2 pounds of pure bodyfat lost (or however much it is) may not seem that significant when you look at all the other factors that influence weight at the end of using a product like this....but in reality, 2 lbs of bodyfat lost with no changes in muscle is extremely impressive in my opinion...just maybe not the most noticable. combine it with some caffeine and 1,3 dma and the testimonials would be awesome.

[BringnIt]

yes. other issues could be a lack of 3,5'-T2 which is more active than 3,3'-T2 to my understanding. my guess is that you simply did not notice the results. just because it is a thyroidal compound doesnt mean it will increase your metabolic rate and have the other expected benefits of T3. we see here that it has been shown to have activity in brown adipose tissue. i am willing to bet that if you were to measure body fat with a precise mechanism, you would have seen a decrease (given a caloric maintenance). the 2 pounds of pure bodyfat lost (or however much it is) may not seem that significant when you look at all the other factors that influence weight at the end of using a product like this....but in reality, 2 lbs of bodyfat lost with no changes in muscle is extremely impressive in my opinion...just maybe not the most noticable. combine it with some caffeine and 1,3 dma and the testimonials would be awesome.

I typically stacked them with stimulants, in the case of Mitotropin it was ran with ephedrine hcl. Mito is also a blend of 3,3 and 3,5. I just didn't notice anything above and beyond typical EC stacks, although I will definitely concede that more accurate testing could've showed more substantial results than I noticed.

So you think the primary mode of action would be through activation of BAT fat, as opposed to an increase in metabolic rate? That doesn't seem like it'd be worth the coin in humans.

[michael3435]

I typically stacked them with stimulants, in the case of Mitotropin it was ran with ephedrine hcl. Mito is also a blend of 3,3 and 3,5. I just didn't notice anything above and beyond typical EC stacks, although I will definitely concede that more accurate testing could've showed more substantial results than I noticed.

So you think the primary mode of action would be through activation of BAT fat, as opposed to an increase in metabolic rate? That doesn't seem like it'd be worth the coin in humans.

i dont think it increases the metabolic rate at all, which makes it a great compound to stack with stimulants. but yeah, you wont "notice" anything really until you look at the before and after results or until you take measurements.

it probably has other effects we dont know about yet. i think something that target brown adipose tissue is awesome imo. i think that if you find ingredients like forskolin valuable, then this is right up your alley.

[BringnIt]

i dont think it increases the metabolic rate at all, which makes it a great compound to stack with stimulants. but yeah, you wont "notice" anything really until you look at the before and after results or until you take measurements.

it probably has other effects we dont know about yet. i think something that target brown adipose tissue is awesome imo.

Cool, I appreciate the responses. Perhaps I will look into a different product that way I can more precisely dose it and see if I feel more positively about it this go around. Getting to that point of the diet where fat loss is becoming more difficult.

[michael3435]

Cool, I appreciate the responses. Perhaps I will look into a different product that way I can more precisely dose it and see if I feel more positively about it this go around. Getting to that point of the diet where fat loss is becoming more difficult.

np man. good luck hope it works out for you.

[NO HYPE]

where did you get this info? source number 4 shows that neither metabolite causes any significant suppression of TSH. this might be different for thyroacetic acids.

Life Sci. 1998;62(26):2369-77.
Moreno M, Lombardi A, Lombardi P, Goglia F, Lanni A.
Effect of 3,5-diiodo-L-thyronine on thyroid stimulating hormone and growth hormone serum levels in hypothyroid rats.

We have investigated the biological effects of physiological doses of 3,5-diiodo-L-thyronine (3,5-T2) and 3,3'-diiodo-L-thyronine (3,3'-T2) (at doses from 2.5 to 10 microg/100 g BW) on serum TSH and GH levels in rats made hypothyroid by propylthiouracil and iopanoic acid administration. In such animals deiodinase activities were inhibited and thyroid hormones serum levels strongly reduced. The effects of T2s were compared with those elicited by 3,5,3'-triiodo-L-thyronine (T3) (2.5 microg/100 g BW).The serum TSH level was much greater in hypothyroid rats than in euthyroid ones. T3 administration suppressed TSH by 88% compared to control (i.e, the level in hypothyroid rats); it thus reached a value not significantly different from that seen in the euthyroid rats. 3,5-T2 produced a similar effect, suppressing the TSH level by about 75% compared to control; it thus reached values not significantly different from those of the euthyroid and T3-treated rats. By contrast, 3,3'-T2 had no effect on TSH, whatever the dose. The serum GH level was much lower in hypothyroid rats than in euthyroid ones. T3 administration increased the GH level by about 5-fold, restoring it to the value seen in euthyroid rats. 3,5-T2-treated hypothyroid rats, at all the doses used (from 2.5 to 10 microg/100 g BW), showed increased serum GH levels: at a dose of 10 microg/100 g BW the level reached a value about 5-fold higher than that in hypothyroid rats. This value was not significantly different from those of euthyroid and T3-treated rats. 3,3'-T2 did not affect GH levels whatever the dose. Thus, 3,5-T2 (but not 3,3'-T2) seems to mimic the effects of T3 on serum TSH and GH levels in rats.


J Endocrinol. 1995 May;145(2):291-7.
Horst C, Harneit A, Seitz HJ, Rokos H.
3,5-Di-iodo-L-thyronine suppresses TSH in rats in vivo and in rat pituitary fragments in vitro.

3,5-Di-iodo-L-thyronine (T2) is a naturally occurring metabolite of thyroxine (T4). Contrary to earlier findings, T2 has recently been shown to have rapid effects in rat liver and in mononuclear blood cells. In the experiments described here, T2 was tested to determine whether it has a TSH suppressive effect in rats in vivo and in rat pituitary fragments in vitro. In experiments over 2 weeks in rats in vivo, low doses of T2 (20-200 micrograms/100 g body weight per day) had no significant influence on body and organ weights, but significantly decreased TSh and T4 serum concentrations. At 200 micrograms/100 g per day, T2 suppressed TSH to 43% and T4 to 29% of control levels. At 1-15 micrograms/100 g per day, 3,5,3'-tri-iodo-L-thyronine (T3), used as a comparison to T2, had significant effects on TSH and T4 levels, and also on body weight. Fifteen micrograms T3/100 g per day decreased TSH to 44%, T4 to 25%, and body weight to 59% of control levels. In experiments over 3 months in rats in vivo, a low dose (25 micrograms/100 g per day) of T2 suppressed TSH to 60% and T4 to 57% of control levels and had no significant influence on other parameters. Conversely, 0.1 microgram/100 g per day T3 had significant effects on body and organ weights as well as pellet intake, but a less pronounced TSH suppressive effect: TSH concentrations were unchanged and T4 concentrations were down to 80% of control values.

[BringnIt]

Life Sci. 1998;62(26):2369-77.
Moreno M, Lombardi A, Lombardi P, Goglia F, Lanni A.
Effect of 3,5-diiodo-L-thyronine on thyroid stimulating hormone and growth hormone serum levels in hypothyroid rats.

We have investigated the biological effects of physiological doses of 3,5-diiodo-L-thyronine (3,5-T2) and 3,3'-diiodo-L-thyronine (3,3'-T2) (at doses from 2.5 to 10 microg/100 g BW) on serum TSH and GH levels in rats made hypothyroid by propylthiouracil and iopanoic acid administration. In such animals deiodinase activities were inhibited and thyroid hormones serum levels strongly reduced. The effects of T2s were compared with those elicited by 3,5,3'-triiodo-L-thyronine (T3) (2.5 microg/100 g BW).The serum TSH level was much greater in hypothyroid rats than in euthyroid ones. T3 administration suppressed TSH by 88% compared to control (i.e, the level in hypothyroid rats); it thus reached a value not significantly different from that seen in the euthyroid rats. 3,5-T2 produced a similar effect, suppressing the TSH level by about 75% compared to control; it thus reached values not significantly different from those of the euthyroid and T3-treated rats. By contrast, 3,3'-T2 had no effect on TSH, whatever the dose. The serum GH level was much lower in hypothyroid rats than in euthyroid ones. T3 administration increased the GH level by about 5-fold, restoring it to the value seen in euthyroid rats. 3,5-T2-treated hypothyroid rats, at all the doses used (from 2.5 to 10 microg/100 g BW), showed increased serum GH levels: at a dose of 10 microg/100 g BW the level reached a value about 5-fold higher than that in hypothyroid rats. This value was not significantly different from those of euthyroid and T3-treated rats. 3,3'-T2 did not affect GH levels whatever the dose. Thus, 3,5-T2 (but not 3,3'-T2) seems to mimic the effects of T3 on serum TSH and GH levels in rats.


J Endocrinol. 1995 May;145(2):291-7.
Horst C, Harneit A, Seitz HJ, Rokos H.
3,5-Di-iodo-L-thyronine suppresses TSH in rats in vivo and in rat pituitary fragments in vitro.

3,5-Di-iodo-L-thyronine (T2) is a naturally occurring metabolite of thyroxine (T4). Contrary to earlier findings, T2 has recently been shown to have rapid effects in rat liver and in mononuclear blood cells. In the experiments described here, T2 was tested to determine whether it has a TSH suppressive effect in rats in vivo and in rat pituitary fragments in vitro. In experiments over 2 weeks in rats in vivo, low doses of T2 (20-200 micrograms/100 g body weight per day) had no significant influence on body and organ weights, but significantly decreased TSh and T4 serum concentrations. At 200 micrograms/100 g per day, T2 suppressed TSH to 43% and T4 to 29% of control levels. At 1-15 micrograms/100 g per day, 3,5,3'-tri-iodo-L-thyronine (T3), used as a comparison to T2, had significant effects on TSH and T4 levels, and also on body weight. Fifteen micrograms T3/100 g per day decreased TSH to 44%, T4 to 25%, and body weight to 59% of control levels. In experiments over 3 months in rats in vivo, a low dose (25 micrograms/100 g per day) of T2 suppressed TSH to 60% and T4 to 57% of control levels and had no significant influence on other parameters. Conversely, 0.1 microgram/100 g per day T3 had significant effects on body and organ weights as well as pellet intake, but a less pronounced TSH suppressive effect: TSH concentrations were unchanged and T4 concentrations were down to 80% of control values.

What are your views on the best forms of thyroid metabolites, mechanisms of action, and potential rebound effects from use?

[michael3435]

Life Sci. 1998;62(26):2369-77.
Moreno M, Lombardi A, Lombardi P, Goglia F, Lanni A.
Effect of 3,5-diiodo-L-thyronine on thyroid stimulating hormone and growth hormone serum levels in hypothyroid rats.

We have investigated the biological effects of physiological doses of 3,5-diiodo-L-thyronine (3,5-T2) and 3,3'-diiodo-L-thyronine (3,3'-T2) (at doses from 2.5 to 10 microg/100 g BW) on serum TSH and GH levels in rats made hypothyroid by propylthiouracil and iopanoic acid administration. In such animals deiodinase activities were inhibited and thyroid hormones serum levels strongly reduced. The effects of T2s were compared with those elicited by 3,5,3'-triiodo-L-thyronine (T3) (2.5 microg/100 g BW).The serum TSH level was much greater in hypothyroid rats than in euthyroid ones. T3 administration suppressed TSH by 88% compared to control (i.e, the level in hypothyroid rats); it thus reached a value not significantly different from that seen in the euthyroid rats. 3,5-T2 produced a similar effect, suppressing the TSH level by about 75% compared to control; it thus reached values not significantly different from those of the euthyroid and T3-treated rats. By contrast, 3,3'-T2 had no effect on TSH, whatever the dose. The serum GH level was much lower in hypothyroid rats than in euthyroid ones. T3 administration increased the GH level by about 5-fold, restoring it to the value seen in euthyroid rats. 3,5-T2-treated hypothyroid rats, at all the doses used (from 2.5 to 10 microg/100 g BW), showed increased serum GH levels: at a dose of 10 microg/100 g BW the level reached a value about 5-fold higher than that in hypothyroid rats. This value was not significantly different from those of euthyroid and T3-treated rats. 3,3'-T2 did not affect GH levels whatever the dose. Thus, 3,5-T2 (but not 3,3'-T2) seems to mimic the effects of T3 on serum TSH and GH levels in rats.


J Endocrinol. 1995 May;145(2):291-7.
Horst C, Harneit A, Seitz HJ, Rokos H.
3,5-Di-iodo-L-thyronine suppresses TSH in rats in vivo and in rat pituitary fragments in vitro.

3,5-Di-iodo-L-thyronine (T2) is a naturally occurring metabolite of thyroxine (T4). Contrary to earlier findings, T2 has recently been shown to have rapid effects in rat liver and in mononuclear blood cells. In the experiments described here, T2 was tested to determine whether it has a TSH suppressive effect in rats in vivo and in rat pituitary fragments in vitro. In experiments over 2 weeks in rats in vivo, low doses of T2 (20-200 micrograms/100 g body weight per day) had no significant influence on body and organ weights, but significantly decreased TSh and T4 serum concentrations. At 200 micrograms/100 g per day, T2 suppressed TSH to 43% and T4 to 29% of control levels. At 1-15 micrograms/100 g per day, 3,5,3'-tri-iodo-L-thyronine (T3), used as a comparison to T2, had significant effects on TSH and T4 levels, and also on body weight. Fifteen micrograms T3/100 g per day decreased TSH to 44%, T4 to 25%, and body weight to 59% of control levels. In experiments over 3 months in rats in vivo, a low dose (25 micrograms/100 g per day) of T2 suppressed TSH to 60% and T4 to 57% of control levels and had no significant influence on other parameters. Conversely, 0.1 microgram/100 g per day T3 had significant effects on body and organ weights as well as pellet intake, but a less pronounced TSH suppressive effect: TSH concentrations were unchanged and T4 concentrations were down to 80% of control values.

i would take rat data on thyroid suppression with a grain of salt.

3,5-Diiodo-L-thyronine (T2) has selective thyromimetic effects in vivo and in vitro
SG Ball, J Sokolov, and WW Chin


Recent data have suggested that the iodothyronine, 3,5-diiodo-l-thyronine (T2), has selective thyromimetic activity. In vivo, T2 has been shown to suppress TSH levels at doses that do not produce significant peripheral manifestations of thyroid hormone activity. Furthermore, T2 has been shown to produce smaller increments in peripheral indices of thyroid status than does T3, when doses resulting in equivalent suppression of circulating TSH are compared. We have assessed the selective thyromimetic activity of T2 in vivo and in vitro, and performed in vitro studies to assess the potential molecular basis for these selective properties. T2 was 100-fold less potent than T3 in stimulating GH mRNA levels in GH3 cells. In contrast, the iodothyronines were almost equivalent in their ability to downregulate TRbeta2 mRNA levels in this cell line. Both 3,3'-diiodo-L-thyronine and thyronine exhibited no significant thyromimetic effects on either process. In vivo, doses of T2 and T3 that were equivalent in their induction of hepatic malic enzyme (ME) mRNA did not produce equivalent suppression of circulating TSH, with T2 being only 27% as effective as T3. T2 was up to 500-fold less potent than T3 in displacing [125I]-T3 from in vitro translated specific nuclear receptors (TRs) and GH3 cell nuclear extracts. Electrophoretic mobility shift assays, assessing the ability of T2 to produce dissociation of TRbeta1 homodimers from inverted palindrome T3 response elements, indicated that T2 was also 1000-fold less potent than T3 in this respect. These data confirm that T2 has significant thyromimetic activity, and that this activity is selective both in vivo and in vitro. However, there are no data to support a selective central effect, T2 being relatively more potent in stimulating hepatic ME mRNA than in suppression of TSH in vivo. The basis for this differential thyromimetic activity is not selective affinity of the different TR isoforms for T2, or divergent properties of T2 in competitive binding and functional assays in vitro.



500-fold less suppression than 3,5-T3 is nothing to worry about and 3,3'-T2 is even weaker. let me read the full texts of what you posted and then i will be able to better comment. i ran across a good amount of literature suggesting there is no suppression issue with 3,5-T2....i think you'd agree 3,3'-T2 isnt a problem.