Experiments

Does topical JXL-069 produce visible regrowth, greater density or thicker hair beyond the shedding control I observed with RU58841?

Why it matters: JXL-069, also indexed as suvomipic and PP405, targets follicle metabolism through mitochondrial pyruvate carrier inhibition. This active record follows regrowth and hair quality separately from shedding, with the first application date, actual exposure and personal observations still to be recorded.

Does topical KX-826 maintain the shedding control I observed with RU58841 and add a visible improvement in density or hair thickness?

Why it matters: Pyrilutamide blocks androgen signaling at the receptor. A 2026 phase III trial reported improved non-vellus hair counts with both 0.5% and 1% formulations. This active record separates hair retention from growth, with the first application date, actual exposure and personal observations still to be recorded.

Does 27 days of Halo Elite at a planned three tablets daily improve repeatable two-set lifting performance at the same load and effort on top of my existing routine?

Why it matters: The active experiment has a nine-day baseline scheduled for October 23 to 31, intervention from November 1 to 27, and follow-up through December 15. Legs, push and pull anchors provide matched performance comparisons; bodyweight, tape measurements, recovery and blood pressure provide context. First use is not yet recorded, and no result has been assigned.

Does eight weeks of Safralis at 15 mg twice daily produce a worthwhile improvement in overall mood, enjoyment or stress tolerance while preserving daytime alertness?

Why it matters: The experiment is active, with pre-start observations collected October 20 and dosing scheduled from October 21 through December 15, followed by two weeks off-product through December 29. Overall mood is primary; enjoyment, stress reactivity, daytime sleepiness, WHO-5 well-being and existing WHOOP sleep data provide context. First ingestion is not yet confirmed.

Across a three-week course around international travel, does Endoluten plus Crystagen produce a meaningful change in sleep, jet lag, recovery, or immune blood markers?

Why it matters: Endoluten supplies the pineal/circadian hypothesis and Crystagen the immune hypothesis. Both started October 5 at one capsule with breakfast and one with dinner, with the final day planned for October 25. Baseline bloodwork was collected before the first capsules; follow-up is planned for October 29, alongside WHOOP and daily observations.

After a one-night tolerance test, do nine nights at 300 mg lower urinary F2-isoprostanes, a marker of lipid oxidation, while liver markers stay in range?

Why it matters: At hundreds of milligrams, melatonin is studied for antioxidant effects rather than sleep. A 300 mg/day ALS study reported oxidative-damage markers returning to control values, and a 2026 trial at the same dose was stopped after liver-enzyme rises. Night 1 was well tolerated; the block runs in late October with bloodwork before and after.

Over consistent daily use, does 20 mg of lutein plus 4 mg of zeaxanthin produce a noticeable improvement in glare tolerance or visual recovery during night driving?

Why it matters: Lutein and zeaxanthin accumulate in the macula and can increase macular pigment. My practical reason for testing them is imperfect glare tolerance during night driving, which I attribute mainly to astigmatism. The supplement will not correct that refractive error; the narrower question is whether glare recovery or contrast improves subtly over time.

At 15 mg every morning while fasted, do the lipid effects reported in human Cardarine trials show up in my bloodwork?

Why it matters: The first Cardarine run produced no meaningful endurance, training-feel, or recovery benefit. This new run asks a different question: whether ApoB, LDL cholesterol, HDL cholesterol, and triglycerides change. The earlier no-signal result remains a separate completed record.

At 5 mg every morning while fasted, does the clear visual body-fat reduction from the earlier run repeat, including the stronger response during the first two weeks?

Why it matters: The first run was helpful: body fat visibly decreased without an acute training effect. This repeat records the early response and whether it slows again, using visual comparisons, waist, and weight trend while the current metabolic routine remains part of the context.

Does 1,000 mg every other day post-workout help maintain energy and training output alongside ATX-304, SANA, and BAM15?

Why it matters: Carnitine participates in mitochondrial fatty-acid transport. The experiment asks whether greater availability helps in this routine, with usable energy and subsequent training performance as the main readout. It replaces the earlier oral L-tartrate fat-loss proposal.

After a 14-day measurement baseline, does 2.5 mg/day of oral TAK-653 add a repeatable improvement in vigilant attention, mental clarity, sustained engagement, or cognitive fatigue on top of stable Bromantane use without worsening sleep, blood pressure, anxiety, activation, or headache?

Why it matters: TAK-653 is a selective AMPA-receptor positive allosteric modulator with demonstrated human target engagement and a positive Phase 2 depression signal, but little direct evidence of cognitive enhancement in healthy people. This experiment uses one fixed pre-dose three-minute morning vigilance test, evening subjective ratings, WHOOP sleep, and blood pressure while excluding Modafiendz and other new cognitive interventions.

At the current 400 mg/day exposure, split into two 200 mg oral doses, does ATX-304 produce a meaningful change in body composition or metabolic markers, and what happens to exercise energy, training quality, temperature, heart rate, and recovery?

Why it matters: ATX-304 combines broad peripheral AMPK activation with increased mitochondrial proton leak. Early human research reported changes in resting metabolic rate, liver fat, visceral fat, triglycerides, and adiponectin, but it did not establish weight-loss efficacy or athletic performance in healthy trained people. This experiment records whether that metabolic signal becomes personally observable while the overlap with other active metabolic compounds remains explicit.

Does 1,500 mg/day of oral BAM15, split between post-workout, after the daily large meal, and before sleep, produce a meaningful fat-loss or body-composition result without an unacceptable change in temperature, resting heart rate, training performance, or recovery?

Why it matters: BAM15 directly reduces mitochondrial calorie-to-ATP efficiency and produced a strong, repeatable fat-loss signal in mouse models. The exposure was titrated upward to pursue greater benefit, and the first dose moved from after waking to post-workout after the earlier timing produced low training energy.

Can NP Thyroid plus T3 bring my free T3 back to my earlier 2026 range during a sustained calorie deficit, and does that change daily energy or the rate of fat loss?

Why it matters: NP Thyroid alone did not keep free T3 in range during my cut: it was 2.1 pg/mL on 15 mg and 1.7 on 30 mg. Adding 25 mcg T3 on October 7 raised it to 2.6 by October 19. I am now moving to 40 mcg T3, aiming for about 3.0 within the reference range.

Does increasing oral SLU-PP-915 from 20 mg to 30 mg daily after waking provide additional benefits in exercise energy, cardio capacity, or training output, with weight loss as a secondary result?

Why it matters: SLU-PP-915 is an orally active pan-ERR agonist that increased aerobic exercise capacity and mitochondrial exercise-response markers in mice. The experiment tests whether that preclinical energy story becomes a repeatable training result, while also watching weight and body composition.

After titrating to 400 mg after waking and 400 mg before sleep (800 mg/day total), what changes in body temperature and sweating, and does SANA (MVD1) produce a visible fat-loss or body-composition result?

Why it matters: CL-316243 produced a helpful visual fat-loss result through a beta-3 adrenergic approach. SANA tests a different thermogenic mechanism built around creatine-dependent energy expenditure rather than a perceptible stimulant effect or appetite suppression.

During a seven-day run at 10 mg per day, does it produce a repeatable change in recovery, immune resilience, inflammation, sleep, or general well-being?

Why it matters: This is a short thymic-peptide experiment built around claims involving immune aging, T-cell signaling, and gene-expression changes. The useful test is whether anything measurable or consistently noticeable changes during the run.

An oral beta-3 adrenergic receptor agonist with human evidence of brown-fat activation and improved glucose handling. A four-week study at 100 mg per day reported increased brown-fat activity and insulin sensitivity, but no change in weight or body composition. The distinction between thermogenesis and a visible fat-loss result is what makes this worth investigating.

Why it is interesting: My planned experiment is 100 mg per day for four weeks, after the CL-316243 experiment finishes, with no overlap between the two. It remains queued, with no start date or results yet. The matching human study used extended-release tablets; 100 mg is above the approved adult maximum of 50 mg, and increased heart rate and blood pressure were reported. Dose, formulation, and monitoring need prescriber review before starting.

An oral deproteinized calf-blood preparation discussed in nootropic communities for mental energy and reduced brain fog. The proposed tablet course comes from community-guide dosing, while the larger cognitive trials studied people with neurological impairment.

Why it is interesting: The planned experiment is 1,200 mg per day orally, divided into 400 mg three times daily using 200 mg tablets, for 4–6 weeks. The useful question is whether it improves mental clarity, sustained reading or work capacity, and cognitive fatigue against a stable surrounding routine. This remains a queued personal nootropic experiment, with no start date or results yet; the proposed course is not an established protocol for healthy cognitive enhancement.

MemoProve is the oral N-PEP-12 peptide-and-amino-acid preparation derived from the same development lineage as Cerebrolysin. A 2026 randomized, double-blind trial in 276 adults with subjective cognitive complaints reported exploratory day-90 advantages in attention and working-memory outcomes at 45 mg and 90 mg, although the combined model did not show an overall treatment-arm main effect. The commercial tablet contains 90 mg of N-PEP-12; the 425 mg figure in some catalog listings is the tablet weight, not the active amount.

Why it is interesting: The proposed experiment is one 90 mg tablet at the same time daily for 90 days, preceded by a 14-day stable baseline and followed by 28 days off-product. With the Cerebrolysin experiment now closed, it can begin after the surrounding cognitive routine is stable. The useful result must extend beyond a vague feeling: at least one fixed attention or working-memory measure should improve beyond baseline variability, remain improved through most of the final four weeks, and agree with a practical change in focus, cognitive fatigue, or work output without a meaningful sleep, anxiety, mood, or tolerability penalty.

A long-studied racetam with substantial human exposure and plausible cholinergic-glutamatergic activity. Older trials reported mixed cognitive results in dementia, while a small healthy-volunteer study found that it partially reversed scopolamine-induced memory impairment. That establishes possible anti-amnesic activity, not enhancement of normal cognition.

Why it is interesting: This is a memory-and-learning candidate rather than a conventional stimulant. The useful question is whether ordinary oxiracetam can produce a repeatable signal in an unimpaired person instead of merely counteracting cognitive dysfunction. The caution is that direct healthy-cognition evidence is limited to a 12-person induced-amnesia study, a recent 500-person post-stroke trial was negative, and newer traumatic-brain-injury evidence primarily favored the isolated active enantiomer over conventional oxiracetam. Its predominantly renal elimination and poorly characterized stack interactions also matter.

LDN keeps coming up as a possible immune, inflammation, pain, mood, and recovery lever.

Why it is interesting: The possible upside is not direct muscle growth. The interesting angle is whether reducing inflammatory drag could improve recovery quality, pain tolerance, sleep stability, training consistency, and how well the rest of the stack feels.

A prescription low-dose insomnia treatment aimed specifically at sleep maintenance. It fits the current pattern: falling asleep reliably, then waking after roughly five hours, with the goal of extending total sleep toward six to seven hours rather than adding more help at sleep onset.

Why it is interesting: This would be a future, prescriber-guided single-variable sleep experiment. The useful question is whether 3 mg reduces early-morning waking and extends sleep without next-day grogginess or impaired alertness. I would judge it by sleep-onset-to-final-waking time, wake time after sleep onset, total sleep, and how I feel the next morning. It would be evaluated as an isolated switch, not stacked with seltorexant or another sleep medication.

A non-sedating amino acid associated with relaxed wakefulness and modest improvements in subjective sleep quality, sleep latency, and daytime function in human trials. It is a plausible way to test whether lowering pre-sleep mental arousal improves sleep without using another sleep medication, although the clearest sleep evidence generally uses lower amounts than the planned experiment.

Why it is interesting: This would be a future single-variable sleep experiment starting at 500 mg before sleep, with the option to increase to 1 g as a separate dose phase. The useful question is whether either amount produces a repeatable improvement in sleep onset, continuity, total sleep, or next-morning recovery without grogginess, headache, dizziness, unusually vivid dreams, or worse sleep. The 1 g ceiling is an experimental dose-response test rather than an evidence-backed sleep protocol, so the surrounding bedtime stack would remain stable and the two dose phases would be evaluated separately.

A retro-inverso D-peptide myostatin inhibitor that maps directly to the muscle-growth brake side of the problem. Small mouse studies found substantial growth in the specific muscle receiving MID-35, and the 2026 follow-up found that the local hypertrophy remained measurable 12 weeks after one injection.

Why it is interesting: The proposed future experiment is 2.5 mg delivered locally by intramuscular injection into lagging body parts twice per week, with the specific goal of increasing size in the treated muscle rather than producing whole-body growth. That planned exposure is a personal hypothesis, not a human regimen derived from the research: MID-35 has never been studied in people, and 2.5 mg is about 1,063 nmol, roughly 532 times the absolute 2 nmol used in the 2026 local mouse study. There is no validated way to scale that tissue dose to a person. The allocation of the 2.5 mg across multiple body parts, experiment duration, and stopping rules remain to be defined before the experiment starts.

A pharma-developed, nonsteroidal selective androgen receptor modulator with controlled human data showing lean-mass increases and a disease-population strength signal. Among the anabolic candidates, it stands out because the evidence base is cleaner than gray-market SARM marketing and stronger than cell-only or mouse-only mechanisms.

Why it is interesting: This is the best pharma-grade human signal in the current anabolic backlog. The hypothesis is not myostatin-brake removal; it is whether a more clinically studied androgen-receptor signal could add lean-mass leverage without unacceptable tradeoffs. The known concern set is exactly why it stays in future status: HDL suppression, transient liver enzyme elevations, testosterone and SHBG changes, no approval for human use, and unclear long-term risk in a trained healthy person.

An 11-amino-acid, erythropoietin-derived peptide with randomized human evidence in sarcoidosis- and diabetes-associated small-fiber neuropathy. The strongest Phase 2 trial found that 4 mg per day for 28 days increased corneal nerve-fiber area and regenerating GAP-43-positive skin fibers, giving this a more credible nerve-repair signal than a generic tissue-recovery claim. Pain relief was less consistent, and the 1 mg and 8 mg groups did not reproduce the significant corneal result seen at 4 mg.

Why it is interesting: The experiment will use 4 mg per day by subcutaneous injection for 28 days, matching the most studied human regimen. The strongest human endpoints (corneal microscopy, skin biopsy, and formal sensory testing) are not practical at-home measures. Generic recovery, soreness, or wearable data will not show whether nerve repair occurred, but the randomized human nerve-regeneration signal still makes the exposure worth running even if nothing is noticeable. The record can document tolerability and subjective changes while acknowledging that an unnoticed biological effect would remain unmeasured. There is no completed Phase 3 program, and the published human safety record is limited mainly to four-week exposure, with only eight participants completing the longer 12-week study.

A nicotinamide N-methyltransferase inhibitor discussed as a way to reduce NAD+ drain and shift metabolic signaling, mostly from preclinical obesity and metabolism work.

Why it is interesting: This is the NAD+ efficiency-multiplier idea. If the mechanism matters, the relevant outcomes would be body composition, metabolic flexibility, nutrient partitioning, and keeping energy metabolism cleaner while training hard.

A synthetic REV-ERB-alpha/beta agonist, not a SARM, used in research around circadian-clock regulation, energy expenditure, lipid metabolism, inflammation, immune-cell metabolism, cancer-cell autophagy, and senescence. That mechanism explains why it gets marketed around fat loss, endurance, and recomp, but the useful evidence is mainly preclinical and mechanistic rather than approved human-use data.

Why it is interesting: Mechanistically, this sits in the recomp neighborhood because REV-ERB signaling touches circadian metabolism, fuel use, and energy expenditure. My interpretation is much more cautious than with ATX-304: it is an interesting research chemical, not a clean body-recomp tool. The concerns are the weak human-use footing, possible circadian disruption, broad effects on core clock biology, and WADA-prohibited status. If it ever became relevant, it would need a high bar and objective markers, not fat-loss marketing claims.