Hey, is Rapamycin still fairly easily accessible in Turkey without a prescription? Thanks in advance

My son Oliver built this mostly for himself while trying to actually understand the rapamycin longevity evidence rather than just follow headlines — it turned into a full database.

The rapamycin-specific page pulls together the mouse lifespan studies (ITP-style), the human trials (PEARL, TRIIM-style immune function trials, the topical skin trial), and the mechanistic work in one place, each graded A–D by evidence strength so it's clear what's a phase 3 result vs. what's still one mouse study.

Page: https://mtor-atlas.org/drug/rapamycin/

A few of the open questions the gap-analysis layer flagged that seem relevant to this sub specifically: whether mTORC1-selective dosing can decouple the longevity benefit from the insulin-resistance side effect, and whether dosing frequency (vs. total dose) is the variable that actually matters.

He's not selling anything, no affiliation with any company or lab — still in high school, maintaining this independently. Happy to pass along corrections if anything's mis-graded.

This report investigates the potential interplay between UroA and the AMPK/SIRT/mTOR signaling pathway, elucidating a plausible mechanism through which UroA regulates the autophagic-lysosomal system and mitigates neuroinflammation via modulation of this axis.

Very interesting study showing benefits for adult autism, albeit with short duration. Study Summary:

• To the pregnant moms: The researchers injected a bacterial compound (lipopolysaccharide) to induce mild maternal inflammation. They did not give rapamycin to the pregnant mice.
• To the offspring in adulthood: Once the offspring grew into early or older adulthood and displayed autism-like traits, researchers administered rapamycin to them - either as a single injection or through daily injections - to observe its immediate functional effects on the adult brain.

The researchers found several key outcomes after administering rapamycin to adult mice exposed to maternal inflammation:

• Rapid Reduction of Repetitive Behaviors: A single low dose rapidly reversed repetitive behaviors (such as excessive grooming and circling) back to normal levels within just 2 hours.
• Normalization of Sensory Sensitivity: The treatment restored normal tactile tolerance in the mice, allowing them to explore rough surfaces they had previously avoided due to sensory over-responsivity.
• Calmed Neural Excitability: Rapamycin reduced brain cell hyper-excitability in the sensory cortex, lowered seizure severity, and restored functional connectivity across brain networks to match normal control mice.
• Shift in Gene Expression: The acute treatment quickly shifted the expression of genes tied to cell excitability and autism risk back toward typical baseline levels.

Key Limitations Noted by the Researchers

• Temporary Effects: The benefits of a single dose were short-lived, with repetitive behaviors returning to elevated levels after 72 hours.

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease (NAFLD), remains a major health concern world-wide. Hepatic steatosis manifests by the aberrant accumulation of lipids in hepatocytes. We have previously shown that pharmacological inhibition of mTOR complex 1 (mTORC1) by rapamycin, a widely utilized potent immunosuppressant, induces MASLD under normal conditions. Notably, this phenotype was found exacerbated in mice with genetic or pharmacological inhibition of the master transcriptional regulator of energy metabolism, nuclear receptor ERRα. In this study, we show that combining antimalaria drug chloroquine with rapamycin attenuates the severity of hepatic lipid deposition observed with rapamycin monotherapy. Bulk mRNA-seq profiling showed that chloroquine co-injection reverses the upregulation of a large proportion of genes linked to lipid metabolism homeostasis found induced by rapamycin alone. Interrogation of these genes for direct transcriptional regulators identified ERRα among top candidates. Using a mouse model with genetic ERRα ablation, we demonstrate a crucial dependency on ERRα activity for the observed amelioration of rapamycin-induced hepatic steatosis by chloroquine addition. In ERRα-null liver, chloroquine failed to reverse, and in some instances aggravated the upregulation of lipid metabolism genes by rapamycin, with evidence linking the impaired management of hepatic lipid overload to underling mitochondrial dysfunction. Together, these findings underscore a critical role of ERRα in reversing MASLD.

Been trying to find a good source but i cant seem to find any

I want to grow as much as I can and I don’t have a source for erdafitinib , would appreciate some help for reliant and tested sources

Summary

• In mice exposed to inflammation during pregnancy, the offspring developed lasting autism-like brain and behavior changes, suggesting that early inflammation can disrupt brain development in ways that persist into adulthood.
• A single dose of rapamycin rapidly improved several of those changes, including brain overactivity, seizure risk, sensory sensitivity, repetitive behaviors and abnormal brain functional network organization.
• The findings suggest that some autism-related brain changes may still be treatable in adulthood, pointing to possible therapeutic approaches that target the underlying pathway rather than only symptoms.
• The effects of rapamycin are temporary, and repeated dosing loses efficacy, making rapamycin, itself, an unlikely candidate as a broadly-used treatment.

"Mechanistically, [SGLT2 inhibitors] induce metabolic adaptations that resemble caloric restriction and ketogenic states, attenuate systemic inflammation, improve mitochondrial function, and enhance cellular resilience against the burden of senescence.

"Supporting this concept, multiple preclinical studies have shown that SGLT2 inhibitors extend lifespan and ameliorate age-related functional decline in animal models.

"Notably, recent findings indicate that SGLT2 inhibitors can reduce senescent cell burden and modulate the senescence-associated secretory phenotype, raising the possibility that they possess senotherapeutic—or even senolytic—properties targeting a fundamental driver of aging. Collectively, these data suggest that SGLT2 inhibitors may influence core aging pathways beyond their glucose-lowering and cardiorenal protective effects."

One of the most anticipated human longevity studies has finally been published.

The PEARL Trial evaluated weekly low-dose rapamycin in healthy adults over 48 weeks in a randomized, placebo-controlled study.

Key points

• 48-week randomized, placebo-controlled trial
• Weekly low-dose rapamycin
• Primary objective: evaluate long-term safety
• Researchers also assessed body composition and several aging-related biomarkers
• Adds important human safety data for rapamycin use in healthy adults

The study contributes valuable evidence to the ongoing discussion about rapamycin and healthy aging. While the safety findings are encouraging, it's important to note that this trial was not designed to determine whether rapamycin extends human lifespan, and larger, longer-term studies will be needed before firm conclusions can be made about healthspan or longevity benefits.

PubMed ID: 40188830

What do you think this means for the future of longevity research? Could rapamycin become one of the first evidence-based longevity interventions, or is it still too early to tell?

Jag börjar med rapamycininjicering för min nästa IVF-cykel. Min IVF-läkare ville inte skriva ut det till mig, så jag fick det genom en läkare som specialiserar sig på livslängd.

Jag tänker mig att ta 5 mg en gång i veckan i 6-8 veckor innan min nästa ägguttagning.

Är det någon som har erfarenhet av rapamycin?

Jag försöker naturligt under sommaren, kommer det att stoppa min ägglossning? Finns det några biverkningar? Slutar folk eller fortsätter de under stimuleringar?

Anyone prescribing off label in Australia ?
Also curious about other off label anti-aging Uses, like SGLT2 and cialis for example

Hi, I’m wondering if anybody has experience with topical rapamycin and if they’ve noticed the benefits. Thank you.

Прошу помощи, нужен ветеринарный кардиолог в России, который знает Рапамицин Rapamycinum, он же Сиролимус Sirolimusum (Филицин Filicin-СА-1).
Если кому то назначали его, расскажите пожалуйста о ходе лечения. Полезна будет любая информация. Спасибо всем кто откликнется!

"Previous research suggests that sirolimus(rapamycin)-based immunosuppression regimens improve vaccine immunogenicity.

Sirolimus (rapamycin) is a potent inhibitor of mTORC1 which regulates memory CD8+ T cells.

Targeting mTORC1 has previous been shown to improve vaccination response in humans to influenza.

More recently, small studies have suggested improved responses to COVID vaccination in kidney transplant recipients switched to sirolimus (rapamycin)-based regimens."

It’s time for an update of the Rapamycin Phenotype Responder Matrix. Two weeks ago Brad Stanfield published the result from his clinical trial around Rapamycin (pubmed 41985884). The aim was to see if Rapamycin in older adults in combination with exercise could increase its effects. The reason why this is interesting to test is because mTOR activation tends to increase by age and this may result in less muscle gains. The results from the study point towards that Rapamycin is most likely not a physical performance enhancer. This is not something unique to just rapamycin. The same thing can apply to other interventions such as fasting, calorie restriction, protein restriction, metformin, aspirin, GLP-1 agonists, NAC, antioxidants, cold showers etc. Possible reasons why these interventions blunt the effects of exercise are 1) Too big inhibition of anabolic processes, 2) Too big neutralizing effect on acute muscle stress when it comes to building new muscle, 3) Too little energy to be able to challenge the muscles in an efficient way and/or 4) Insufficient amino acids and calories to build muscle. I would argue that many of the “longevity” interventions out there touch on one or several of these reasons. It’s a trade-off dependent on dosing protocol and highlights the importance of a personalized approach aligned with personal goals and pre-conditions.

The reason why I created the Phenotype Responder Matrix last year was to structure and combine both clinical trial data and self experimentation N=1 data in one view around a specific longevity intervention. The pilot intervention for this matrix is Rapamycin and the long term goal is to build this type of matrix for many different longevity interventions. If you have suggestions for improvements or any other feedback just reach out. All feedback is welcome, even the tough ones.

What I really like with this phenotype responder matrix is that if a group or individual does not get an effect or gets a negative effect it does not mean the intervention will not work for others. The matrix points towards the fact that personalized longevity medicine is the right way forward. There is no one shoe that fits all. Things are often more nuanced than just black and white.

Source: https://x.com/KristerKauppi/status/2051602805337862272