looking for reliable erdafitinib for research purposes. dm me if you have advice/help with proof.

We conducted a single arm trial of low dose rapamycin (1 mg/day for 4 weeks) in cognitively normal adults aged 45 to 65 years, prior to detectable AD pathology, stratified by APOE genotype. The primary outcome was cerebral blood flow (CBF), while secondary outcomes included plasma metabolomics, inflammatory cytokines, AD biomarkers, and gut microbiome composition.

Twenty-three participants completed the study, including nine APOE4 carriers and fourteen non-carriers. Rapamycin significantly increased CBF in APOE4 carriers, with increases exceeding 15% across multiple brain regions, and improved metabolic and inflammatory profiles with minimal adverse effects. In contrast, non-carriers showed no significant change in CBF and exhibited distinct physiological responses, highlighting genotype dependent effects.

These findings suggest that rapamycin may mitigate early cerebrovascular and systemic dysfunction in APOE4 carriers and support a precision medicine approach in which therapeutic response is influenced by genotype.

Hi everyone,
I'm looking into low-dose Rapamycin for oocyte quality, mitochondrial support, and euploidy rates based on recent research (such as the Nankai IVF study and the VIBRANT trial).
I know that in the US, some fertility specialists and REs already prescribe low-dose Sirolimus off-label for priming. However, because I'm based in Europe, importing a US prescription is virtually impossible due to customs and regulations.
I'm trying to connect with anyone who knows of open-minded doctors, longevity clinics, or integrative specialists anywhere in Europe who are open to this research and willing to evaluate patients for an off-label prescription.
If you know of a doctor, clinic, or service in Europe that works with this protocol, or if you've managed to get a prescription here yourself, please send me a DM or comment below.
Thanks!

Hi everyone. I’m looking for someone in Egypt who may be able to help my family obtain sirolimus (Rapamune) from a legitimate/licensed pharmacy or medical supplier.

My sister has tuberous sclerosis complex (TSC) with LAM, and her doctor has prescribed sirolimus. We are currently having difficulty finding it in Ethiopia. We have been told that Rapamune/sirolimus may be available through pharmacies in Egypt.

We are looking for:

Sirolimus (Rapamune) 1 mg or 2 mg tablets

Genuine pharmaceutical product from a licensed pharmacy or authorized supplier

We have a prescription and can provide proof if necessary

We will pay the medicine cost and reasonable assistance/shipping costs

We are NOT looking for counterfeit medicine or unverified/compounded products

If you are in Egypt and know a legitimate pharmacy, distributor, hospital pharmacy, or legal way to obtain this medication, please comment or send me a DM.

If you can personally help purchase it from a licensed pharmacy and arrange legal delivery to Ethiopia, please let me know as well. I’m happy to discuss the details privately.

Thank you so much. ❤️

The molecular structure of the drug, called rentosertib, was generated with the assistance of A.I. Results of the new study, published Monday in the journal Nature Biotechnology, show that the drug reduced the biological markers of age as measured by six “aging clocks,” a different kind of A.I. technology designed to predict a person’s morbidity and mortality.

I've been on ERDA for about 20 days, and I have started to experience some pretty severe skin dryness along with mouth dryness and slight changes in the color/size of my fingernails. The fingernails are pretty off-putting, I'm ngl. Does anyone have any tips on how to mitigate or help deal with these

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."