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Telomeres are non-encoding DNA repeats at the tips of the chromosome. In the picture below they are the little yellow dots:

As our cells divide these tips shorten, typically from 12-15 'kilobase pairs' (kb) to 4kb over a lifetime1, the cells which they inhabit become older and more dysfunctional and reproduce less often2. Finally they hit the ‘Hayflick Limit’ at which point they become ‘senescent' and are unable to divide.

Over a decade ago it was discovered that an enzyme called telomerase can lengthen shortening telomeres. It exists in the body's immortal cells - germ cells and embryonic stem cells - but is not expressed in other cell types in quantities great enough to stop the erosion in them. It was shown that by activating telomerase in these types of cells in vitro they become immortalized, do not age across divisions and divide indefinitely.3 After a long search, a compound was discovered that can activate telomerase, in both mice and humans, both in vitro and in vivo, at substantial levels above 300% of normal4. That compound is TA-65.

A New Era

In our opinion aging is by design and telomere shortening is the mechanism by which that design is carried out. If you agree with us on that, you would probably consider it remarkable that for thousands of years, there has never been a way to lengthen them. As our ancestors labored in the creation of elixirs from alchemy and myth, and as the Egyptian, Roman and countless other empires rose and fell, the telomeres of every living human being on Earth moved inexorably in one direction – down.

Amazingly, those days have ended with this product. For the first time in human history we can - with a simple pill - reverse the process that lies at what we believe to be at the bottom of the cascade of cause and effect that is aging. We can literally reverse the clock of aging and elongate human telomeres5. The catch is that we still cannot elongate telomeres of average length. TA-65 targets critically short telomeres (<4kb) and elongates them only. This is because shorter telomeres preferentially recruit telomerase more easily than longer ones6. There appear to be some mechanisms at work in the cell, particularly involving the 'shelterin' complex that surrounds the telomere like a sheath, which block telomerase access to longer telomeres. The solution to this is to loosen the shelterin, or to overwhelm it with higher levels of telomerase, neither of which have been accomplished to date.

Elongation of telomeres is the first step though in a new era that we believe will eventually culminate in the defeat of aging via periodic controlled extension of telomeres.

Aging Biomarkers

So what is the consequence of lengthening the shortest of telomeres but not the others? The results are that the body is profoundly rejuvenated in many ways.

The cells in your body with the shortest telomeres are the most dysfunctional, the oldest, and are key players in age-related poor tissue function. 7 They do not pull their weight for the team, and in fact often disrupt the otherwise coordinated efforts of their neighbors. At the most extreme case, the cells are senescent and become toxic to surrounding cells. In areas where there has been chronic damage, causing high cell turnover, which leads to shorter telomeres and inferior repair cycles, these critically short telomeres exist in higher proportions than elsewhere and are causing greater damage. So the effects of reducing those cell types from your body, throughout all of your tissues, are potentially far-reaching.

Harley Study

A recent in-vivo human study of TA-65 published in 2010 in Rejuvenation Research entitled A Natural Product Telomerase Activator As part of a Health Maintenance Program showed that the immune system was remodeled, to a profile of someone on average 5-20 years younger. 8

As we age, the relative ratio of white blood cell types changes. The ratio of CD4/CD8 cells, for example, goes down with age. When this ratio falls below one, it is considered an immune risk profile (IRP).9 This ratio change is driven largely by the typical .57% increase in % of CD8+ cells per year as we age. 10 Also, the percentage of Natural Killer cells typically increases .3% per year. 11 In cases where the relative ratio of a white blood cell type goes up, the current theory is that this is done as a compensation for the reduced efficacy of that cell type as it ages12. The TA-65 group in this study however, experienced dramatic decreases after one year in in these cell types of 20% for CD8 and 17% for NK cells. The full effect of the immune system remodeling can be seen below13:

Cell Type TA-65(1 year) General population (one-year)
CD8+CD28 T cells -20% +.57%
Natural Killer (NK) cells -17% +.3%
Neutrophils +6% historically conflicting, Harley et al: depends on CMV status

As you can see the changes in relative white blood cell types are substantial as compared to those changes typically associated with aging, and they were in the other direction. Again, the authors concluded that that represented an age-reversal of 5-20 years for the immune system profile. Particularly striking was the fact that the critically famous CD4/CD8 ratio increased substantially after a year of TA-65 treatment.

Blasco Study

In a subsequent study of the in vivo effects of TA-65 by Maria Blasco using mice entitled The Telomerase Activator TA-65 Enlongates Short Telomeres and Increases Health Span of Adult/Old Mice without Increasing Cancer Incidence, the team confirmed that the critically short telomeres were being lengthened14. They looked much more closely at the effects of various known biomarkers of aging and found that most of them were brought back in time significantly. Blasco's team found that TA-65:

  • Improved glucose absorption and insulin tolerance15
  • Reduced lipid accumulation in the liver.16
  • Rejuvenated skin.17
  • Improved wound healing.18
  • Increased hair growth.19
  • Improved bone density.20
  • Reduced DNA damage.21
  • Reversed age effect of other blood biomarkers RBC and hemoglobin.22
TA-65 does not require a prescription. It is classified as an herbal supplement, and not a drug.

Are There Adverse Effects?

In the Blasco study, the authors concluded that "TA-65 did not show any detectable negative secondary effects, including no increase in incidence of cancer."23 In the Harley study the authors said that "physicians who monitored the health of the current study subjects [] reported no adverse events" and that "no new cases of Cancer or cardiovascular disease were reported"24. However, we do caution our customers that TA-65 is a new and very powerful supplement and little is known about its long term (ie 10 year+) effects in humans.

Will you live longer on TA-65?

The in vivo human study did not cover a long enough time period to understand the impact on human lifespan. The Maria Blasco study on mice found absolutely no increase in either median or maximum life, however. 25 This is not too surprising if we understand that the compound is unable to slow average telomere shortening at this stage. That being the case, then it is defenseless against the overall long term pace of aging, even though it is rejuvenating the function of many tissues due to its ability to lengthen short telomeres.26 In the study, however, the mice were only given TA-65 for 4 months. Perhaps the results would have been different had the administration been continuous.

The Past and Future of Telomerase Activation

Today, there are many people who understand the telomere’s place at the heart of aging. In the 90s, there were far less - only a handful. One of them was Mike West, a charismatic visionary who was given millions in VC funding to start a company on a premise no less ambitious than the discovery of immortality through telomere extension. The result was Geron, a multi-million dollar corporation that sweated and toiled and eventually emerged with, among other things, a compound they proved in a publicly published study would elongate short telomeres in humans - TA-65. And now you can order it on the web and have it shipped to your house.

Not bad for the first 15 years of commercial efforts in telomere biology, wouldn't you say? Stay tuned for the next 15, because they may well include the lengthening of average telomeres. And in the next 50, we should be able to make that happen in stem cells where the elongation really needs to happen for it to 'stick', and throughout all stem cell types, in the correct proportions. When that day comes the Fountain of Youth will have been found. In the meantime TA-65 opens the door for us into a new era. It represents both the beginning of what is to come, as well as a very practical and powerful supplement that you can take today to rejuvenate your body in a more profound sense than has ever happened in human history.

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Product Code: TA65-250-30
Package Quantity: 30 capsules
Shipping Weight: 4.0000 lbs
Serving Size: --

TA-65 Supplement Facts

 Supplement Amount Per Serving % Daily Value
 TA-65 250 IU 


    • 1. Harley et al, 1990. Telomeres shorten during aging of human fibroblasts. Nature 345. 458-460
    • 2.
      Flores I, Benetti R, Blasco MA. Telomerase regulation and stem cell behaviour. Curr Opin Cell Biol 2006;18:254–260.
      Harley CB, Futcher AB, Greider CW. Telomeres shorten during ageing of human fibroblasts. Nature 1990;345:458–460.
    • 3. See this article.
    • 4. Harley et al. 2010. A natural product telomerase activator as part of a health maintenance program. Rejuvenation Research. Volume 14, Number 1.
      Blasco et al. 2011. The telomerase activator TA-65 enlongates short telomeres and increases health span of adult/old mice without increasing cancer incidence. Aging Cell. pgs 604-621
    • 5. Harley et al. 2010. A natural product telomerase activator as part of a health maintenance program. Rejuvenation Research. Volume 14, Number 1.
      Blasco et al. 2011. The telomerase activator TA-65 enlongates short telomeres and increases health span of adult/old mice without increasing cancer incidence. Aging Cell. pgs 604-621.
    • 6. Bianchi A, Shore D (2007) Increased association of telomerase with short telomeres in yeast. Genes Dev. 21, 1726-1730.
      Hemann M, Strong M, Hao L, Greider C. The shortest telomere, not average telomere length, is critical for cell viability and chromosome stability. Cell 2001;107:67–77.
      Samper E, Flores J, Blasco M. Restoration of telomerase activity rescues chromosomal instability and premature aging in Terc mice with short telomeres. EMBO reports 2001;2:800–807.
      Teixeira MT, Arneric M, Sperisen P, Lingner J. Telomere length homeostasis is achieved via a switch between telomerase-extendible and -nonextendible states. Cell 2004;117:323–335.
    • 7. Calado RT, Young NS. Telomere diseases. N Engl J Med 2009;361:2353–2365.0 Hemann M, Strong M, Hao L, Greider C. The shortest telomere, not average telomere length, is critical for cell viability and chromosome stability. Cell 2001;107:67–77.
    • 8. Harley et al. 2010. A natural product telomerase activator as part of a health maintenance program. Rejuvenation Research. Volume 14, Number 1.
    • 9. Strindhall J, Nilsson BO, Lofgren S, Ernerudh J, Pawelec G, Johansson B, Wikby A. No Immune Risk Profile among individuals who reach 100 years of age: Findings from the Swedish NONA immune longitudinal study. Exp Gerontol 2007;42:753–761.
    • 10. Harley et al. 2010. Ibid. Page 8, paragraph 1.
    • 11. Harley et al. 2010. Ibid. Page 9, Figure 4C.
    • 12. "There is broad consensus that NK cell number increases with age to compensate for descreased per-cell activity, which results from impaired signal transduction, but other mechanisms such as decreased barrier function and increased antigenic/pathogenic load may also contribute to increased NK cells with age."
      Harley et al. 2010. Ibid. Page 10, paragraph 3
      "[The typical increase in nuetrophils in CMV- subjects] can be interpreted as a compensatory increase in the face of declining per cell activity and barrier function"
      Harley et al. 2010. Ibid. Page 10, paragraph 1
    • 13. Harley et al. 2010. Ibid. See above for CD8 and NK cell dynamics. For Neutrophils, see page 9 Figure 4B.
    • 14. "TA-65 treatment results in telomerase-dependant elongation of short telomeres"
      Blasco et al. 2011. Ibid. Page 604, paragraph 1.
    • 15. "TA-65 adminsitration during 4 months significantly improved the capacity to uptake glucose after a glucose pulse in the 1-year-old treated mice ompared to control group"
      Blasco et al, 2011. Ibid. Page 610, paragraph 4
    • 16. Telomerase activation in vivo has always been studied and measured only in white blood cells,. In this study the team studied the telomerase expression increases in various tissues, and found a remarkable 10-fold increase in the liver (of mice anyway). This was much higher than other tissue types. It was assumed that this was related to the remarkable ability of the TA-65 mice' liver to resist lipid accumulation typical of old age. "Control mice presented the strongest accumulation of fat in the liver at older ages comparing to the TA-65-treated cohorts, which, together with the previous results, could indicate a liver protective action of TA-65."
      Blasco et al, 2011. Ibid. Page 610, paragraph 5
    • 17. "TA-65 treatment resulted in a significant increase in subcutaneous fat content and epidermal layer in the the one-year old mice, but did not significantly change these parameters in the 2-year-old group" "The epidermis of the TA-65 mice 'showed significantly more proliferating cells, together with significantly reduced numbers of [] apoptotic cells." Blasco, et al. 2011. page 611, paragraph 1.
    • 18. TA65 also improved the in vitro wound healing capacity of keratinocytes, exterior skin cells Blasco, et al. 2011. page 613, Figure 5D.
    • 19. Blasco, et al. 2011. page 613, Figure 5F.
    • 20. "Bone density was improved in in the 2-year old TA65 group compared to controls" Blasco, et al. 2011. Page 611, Paragraph 1.
    • 21. Blasco, et al. 2011. Page 604, Paragraph 1
    • 22. Blasco, et al. 2011. Page 611, Paragraph 2.
    • 23. Blasco, et al. 2011. Page 606, Paragraph 1.
    • 24. Harley, et al. 2010. Page 10, Paragraph 3.
    • 25. Blasco et al. 2011. Ibid. Page 614, paragraph 2
    • 26. Because most cells in our body are constantly dying and being reborn from underlying stem cell pools, it is easy to see how the effect of this rejuvenation once TA-65 has been discontinued might be eventually annulled if TA-65 indeed has no effect on the telomere lengths of the underlying stem cell populations and is only lengthening the telomeres of critically short somatic cells. What the effect of TA-65 is on the underlying stem cell populations is unknown at this time. But if the mice had been given TA-65 continuously during their entire lifetimes, perhaps the continued rejuvenation of their tissues throughout their lives would have resulted in a significant change in lifespan. The authors did declare an increase in 'health span', which was to say that during the same period in which they lived, their organ and tissue function and general biomarkers were all performing at remarkable levels typical of much younger mice.