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Follistatin (FST) is a premier first-line longevity gene therapy because it is well-researched, safe and exceptionally effective. In a recent human clinical trial, FST increased lean mass, decreased fat, decreased inflammation, lengthened telomeres, and dramatically reversed epigenetic age acceleration. Frailty, obesity, and excessive inflammation are hallmarks of aging. In mouse research and in Minicircles human clinical trails, FST safely improves healthy longevity.
It lasts about 1.5 years on average. We envision a model in which patients receive a combination of Minicircle gene therapies annually.
No adverse effects related to therapy were reported in our human clinical trial, and FST has an exceptionally good safety profile in mouse, primate, and human studies. Additionally, Minicircle’s delivery system also has multiple layers of additional safety built in. Our therapy is transient, reversible, and ultimately excisable if necessary.
We turn a small number of bellyfat cells into FST export factories. When these cells export FST into your bloodstream, you get systemic benefits.
There are multiple forms of follistatin. Follistatin-288 causes infertility by binding to and inhibiting actin, thereby decreasing FSH production by the pituitary gland. Follistatin-344 has 10x lower binding affinity and has not been shown in any of our experiments to cause a significant decrease in FSH level. Monkey studies, and male and female human experiments have not shown any effect on fertility hormones or sperm.
Of note in both non-human primate studies and in our subsequent clinical trial we found no effect of FS344 (FS315) gene therapy on any pituitary secreted hormone” (Al-Zaidy, 2015).
NOTE: Follistatin is a new, experimental gene therapy not approved in any nation that less than 200 people in the world are estimated to have taken (as of April 2022).
REFERENCES: 1. Mendell JR, Rodino-Klapac L, Sahenk Z, et al. Gene therapy for muscular dystrophy: lessons learned and path forward. Neurosci Let. 2012;527(2):90-99. doi:10.1016/J.NEULET.2012.04.078 2. Kota J, Handy CR, Haidet AM, et al. Follistatin gene delivery enhances muscle growth and strength in nonhuman primates. Sci Transl Med. 2009;1(6). doi:10.1126/SCITRANSLMED.3000112 3. Lee SJ, McPherron AC. Regulation of myostatin activity and muscle growth. Proc Natl Acad Sci U S A. 2001;98(16):9306-9311. doi:10.1073/PNAS.151270098 4. López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. The Hallmarks of Aging. Cell. 2013;153(6):1194-1217. doi:10.1016/j.cell.2013.05.039 5. Jaijyan DK, Selariu A, Cruz-Cosme R, et al. New intranasal and injectable gene therapy for healthy life extension. Proc Natl Acad Sci U S A. 2022;119(20):1-7. doi:10.1073/pnas.2121499119 6. Gilson H, Schakman O, Kalista S, Lause P, Tsuchida K, Thissen JP. Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin. Am J Physiol - Endocrinol Metab. 2009;297(1):157-164. doi:10.1152/ajpendo.00193.2009 7. Hedger MP, Winnall WR, Phillips DJ, de Kretser DM. The Regulation and Functions of Activin and Follistatin in Inflammation and Immunity. Vol 85. 1st ed. Elsevier Inc.; 2011. doi:10.1016/B978-0-12-385961-7.00013-5 8. Wakatsuki MK, Shintani Y, Saito S, Liu M. Immunoradiometric Assay for Follistatin: Serum Levels in Normal Adults and Pregnant Women. J Clin Endocrinol Metab. 1996;81(2):630-634.
Follistatin (FST) is a premier first-line longevity gene therapy because it is well-researched, safe and exceptionally effective. In a recent human clinical trial, FST increased lean mass, decreased fat, decreased inflammation, lengthened telomeres, and dramatically reversed epigenetic age acceleration. Frailty, obesity, and excessive inflammation are hallmarks of aging. In mouse research and in Minicircles human clinical trials, FST safely improves healthy longevity.
It lasts about 1.5 years on average. We envision a model in which patients receive a combination of Minicircle gene therapies annually.
No adverse effects related to therapy were reported in our human clinical trial, and FST has an exceptionally good safety profile in mouse, primate, and human studies. Additionally, Minicircle’s delivery system also has multiple layers of additional safety built in. Our therapy is transient, reversible, and ultimately excisable if necessary.
We turn a small number of bellyfat cells into FST export factories. When these cells export FST into your bloodstream, you get systemic benefits.
There are multiple forms of follistatin. Follistatin-288 causes infertility by binding to and inhibiting actin, thereby decreasing FSH production by the pituitary gland. Follistatin-344 has 10x lower binding affinity and has not been shown in any of our experiments to cause a significant decrease in FSH level. Monkey studies, and male and female human experiments have not shown any effect on fertility hormones or sperm.
Of note in both non-human primate studies and in our subsequent clinical trial we found no effect of FS344 (FS315) gene therapy on any pituitary secreted hormone” (Al-Zaidy, 2015).
NOTE: Follistatin is a new, experimental gene therapy not approved in any nation that less than 200 people in the world are estimated to have taken (as of April 2022).
REFERENCES: 1. Mendell JR, Rodino-Klapac L, Sahenk Z, et al. Gene therapy for muscular dystrophy: lessons learned and path forward. Neurosci Let. 2012;527(2):90-99. doi:10.1016/J.NEULET.2012.04.078 2. Kota J, Handy CR, Haidet AM, et al. Follistatin gene delivery enhances muscle growth and strength in nonhuman primates. Sci Transl Med. 2009;1(6). doi:10.1126/SCITRANSLMED.3000112 3. Lee SJ, McPherron AC. Regulation of myostatin activity and muscle growth. Proc Natl Acad Sci U S A. 2001;98(16):9306-9311. doi:10.1073/PNAS.151270098 4. López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. The Hallmarks of Aging. Cell. 2013;153(6):1194-1217. doi:10.1016/j.cell.2013.05.039 5. Jaijyan DK, Selariu A, Cruz-Cosme R, et al. New intranasal and injectable gene therapy for healthy life extension. Proc Natl Acad Sci U S A. 2022;119(20):1-7. doi:10.1073/pnas.2121499119 6. Gilson H, Schakman O, Kalista S, Lause P, Tsuchida K, Thissen JP. Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin. Am J Physiol - Endocrinol Metab. 2009;297(1):157-164. doi:10.1152/ajpendo.00193.2009 7. Hedger MP, Winnall WR, Phillips DJ, de Kretser DM. The Regulation and Functions of Activin and Follistatin in Inflammation and Immunity. Vol 85. 1st ed. Elsevier Inc.; 2011. doi:10.1016/B978-0-12-385961-7.00013-5 8. Wakatsuki MK, Shintani Y, Saito S, Liu M. Immunoradiometric Assay for Follistatin: Serum Levels in Normal Adults and Pregnant Women. J Clin Endocrinol Metab. 1996;81(2):630-634.
Follistatin (FST) is a premier first-line longevity gene therapy because it is well-researched, safe and exceptionally effective. In a recent human clinical trial, FST increased lean mass, decreased fat, decreased inflammation, lengthened telomeres, and dramatically reversed epigenetic age acceleration. Frailty, obesity, and excessive inflammation are hallmarks of aging. In mouse research and in Minicircles human clinical trials, FST safely improves healthy longevity.
It lasts about 1.5 years on average. We envision a model in which patients receive a combination of Minicircle gene therapies annually.
No adverse effects related to therapy were reported in our human clinical trial, and FST has an exceptionally good safety profile in mouse, primate, and human studies. Additionally, Minicircle’s delivery system also has multiple layers of additional safety built in. Our therapy is transient, reversible, and ultimately excisable if necessary.
We turn a small number of bellyfat cells into FST export factories. When these cells export FST into your bloodstream, you get systemic benefits.
There are multiple forms of follistatin. Follistatin-288 causes infertility by binding to and inhibiting actin, thereby decreasing FSH production by the pituitary gland. Follistatin-344 has 10x lower binding affinity and has not been shown in any of our experiments to cause a significant decrease in FSH level. Monkey studies, and male and female human experiments have not shown any effect on fertility hormones or sperm.
Of note in both non-human primate studies and in our subsequent clinical trial we found no effect of FS344 (FS315) gene therapy on any pituitary secreted hormone” (Al-Zaidy, 2015).
NOTE: Follistatin is a new, experimental gene therapy not approved in any nation that less than 200 people in the world are estimated to have taken (as of April 2022).
REFERENCES: 1. Mendell JR, Rodino-Klapac L, Sahenk Z, et al. Gene therapy for muscular dystrophy: lessons learned and path forward. Neurosci Let. 2012;527(2):90-99. doi: 10.1016 / J.NEULET.2012.04.078 2. Kota J, Handy CR, Haidet AM, et al. Follistatin gene delivery enhances muscle growth and strength in nonhuman primates. Sci Transl Med. 2009;1(6). doi: 10.1126 / SCITRANSLMED. 3000112 3. Lee SJ, McPherron AC. Regulation of myostatin activity and muscle growth. Proc Natl Acad Sci U S A. 2001;98(16):9306-9311. doi: 10.1073 / PNAS.151270098 4. López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. The Hallmarks of Aging. Cell. 2013;153(6):1194-1217. doi:10.1016/j.cell.2013.05.039 5. Jaijyan DK, Selariu A, Cruz-Cosme R, et al. New intranasal and injectable gene therapy for healthy life extension. Proc Natl Acad Sci U S A. 2022;119(20):1-7. doi: 10.107 3/ pnas.2121499119 6. Gilson H, Schakman O, Kalista S, Lause P, Tsuchida K, Thissen JP. Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin. Am J Physiol - Endocrinol Metab. 2009;297(1):157-164. doi:10.1152/ajpendo.00193.2009 7. Hedger MP, Winnall WR, Phillips DJ, de Kretser DM. The Regulation and Functions of Activin and Follistatin in Inflammation and Immunity. Vol 85. 1st ed. Elsevier Inc.; 2011. doi: 10.1016 / B978-0-12-385961-7.00013-5 8. Wakatsuki MK, Shintani Y, Saito S, Liu M. Immunoradiometric Assay for Follistatin: Serum Levels in Normal Adults and Pregnant Women. J Clin Endocrinol Metab. 1996;81(2):630-634.
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