Does anyone have experience with SLUPP as an injectable? We have a patient injecting a solution of 2ml bac water .5ml of DSMO and 5mg of the SLUPP powder. I am having a hard time finding it in the injectable form through our 503A pharmacy's. Is there a big difference between it and the pill form other than the obvious?

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Good morning everyone!! This came up in one of the groups I am a part of. I wanted to share it here to get Anthony and anyone else who we look to as an expert in this subject matters opinion. I know Anthony’s research contradicts the fact that the member of my group is saying SLU is not bioavailable. But the members research and thoughts are concerning. Can everyone share your thought on this and if there is any validity. I know many a RS has had great results with this compound. The below is copied from the group. SLU-PP is hydrophobic and must be dissolved in chemicals not safe for injection. For oral use, early member tests suggest that SLU-PP does not survive stomach acid and may break down into unsafe byproducts, including hydrazine-like fragments, which should not be ingested by humans. Initial data from Jano on the degradation testing for SLU-PP-332 in simulated stomach acid. https://janoshik.com/tests/87013-SLUPP332_PDDAB_DMSO_HCL_NAOH_H2O_SAMPLE_A_HFW3ZIDG7YN1 https://janoshik.com/tests/87014-SLUPP332_PDDAB_DMSO_HCL_NAOH_H2O_SAMPLE_B_XXH9UD6N8HGF Starting reagents were SLU-PP-332 and p-dimethylaminobenzaldehyde (p-DAB) in DMSO. Sample A was titrated to pH 1.5 with 0.1M hydrochloric acid in water and heated to 37C for 2 hours with constant stirring, then neutralized to pH ~6 with 0.1M sodium hydroxide. Sample B used the same starting reagents, but the heating step was performed without the addition of HCl. Instead, a mixture of 0.1M HCl+NaOH titrated to pH ~6 was added after heating to match the final dilution of sample A. Calculated dilution btw was 1.8mg/mL SLU-PP-332, looks like I got pretty close as sample B tested at 1.719mg/mL. The goal was 2mg/mL but titration is hard and I'm out of practice. Potential breakdown products of SLU-PP-332 are expected to be: 1-napthaldehyde, 4-hydroxybenzohydrazide (4-HBH). The latter can further break down to 4-hydroxybenzoic acid and hydrazine, which will complex with p-DAB to form the yellow azo dye p-dimethylaminobenzalazine. There may also be some complex formed between p-DAB and 4-HBH, I couldn't find this discussed in any literature I could find, though.

Methylene blue is one of the most unusual therapeutic molecules in medicine because it behaves like a living sensor inside the body. It changes color depending on its electron state, donates and accepts electrons depending on mitochondrial demand, bypasses damaged respiratory complexes, and flows directly into the bloodstream, nervous system, and organs as a redox-active dye. While people know it turns urine blue, they rarely understand why that color appears, why the duration changes, and how those changes can reveal meaningful information about mitochondrial efficiency, liver and kidney function, and global redox tone. The truth is that the color shift is not just a cosmetic effect; it is a visible expression of the electron flow inside your cells. The speed at which urine returns to its normal yellow color becomes a rough, experiential marker of how well your body’s redox machinery is cycling. To understand this, the first step is recognizing that methylene blue exists in two major states: its oxidized form (bright blue) and its reduced form, leucomethylene blue, which is colorless. These two forms constantly convert into one another based on the availability of electrons. When methylene blue accepts electrons, it becomes colorless. When it donates electrons, it becomes blue again. This redox cycling is what makes methylene blue so therapeutically valuable it acts like a smart shuttle that smooths out problems in the electron transport chain, especially when complex I or III are underperforming. When mitochondria are stressed, over-reduced, under-fueled, oxidatively burdened, or deprived of NAD+, methylene blue helps buffer the system by accepting excess electrons or donating needed electrons. It reduces oxidative stress, stabilizes the flow of energy, and helps maintain membrane potential. But because it is also a dye, these internal dynamics show up externally, especially in urine. The moment methylene blue enters the bloodstream, the body begins metabolizing it in the liver, reducing it, cycling it, moving it into tissues, and eventually clearing it through the kidneys. The exact hue you see in the toilet depends on two things: how much of the molecule remains in its oxidized blue form versus its reduced colorless form, and how concentrated your urine is. Dark, heavily oxidized methylene blue produces a vivid blue-green color. When most of the MB is reduced and colorless, urine appears normal or lightly tinted. This is why two people taking the same dose can see dramatically different colors. The real insight emerges when you track how long the color lasts.

I’ve talked about this a few times before, but I know there are still plenty of questions around it so I wanted to take another shot at clearly explaining the reasoning behind my answer. The case against higher doses of SLU-PP-332 starts with first principles: this compound works as a signaling cue, not a substrate to be “pushed” toward saturation. In cell systems and animal models, SLU-PP-332 appears to activate the estrogen-related receptor (ERR) program with PGC-1α coactivation, shifting transcription toward fatty-acid oxidation, oxidative phosphorylation, and mitochondrial quality control. That kind of pathway is amplifier biology: a small receptor-level nudge fans out into many downstream genes and post-translational switches. In such networks, more ligand does not linearly equal more benefit; it often crosses into different biology entirely, including compensatory braking and desensitization. Think of it like tapping a conductor’s baton to set tempo versus throwing a bigger baton at the orchestra. The first coordinates; the second creates noise and reflexes you didn’t intend. A key downstream branch of the ERR/PGC-1α program is modulation of uncoupling proteins. Mild, context-appropriate uncoupling in UCP2 and UCP3 can lower electron pressure, trim reactive oxygen species, and improve metabolic flexibility under load. But pushing the axis hard increases the probability of off-site expression and activity in UCP4 and UCP5, which are enriched in neurons and glia. Excess uncoupling in those tissues risks local ATP shortfall where energy security is non-negotiable. In brain and autonomic circuits, too much leak across the inner mitochondrial membrane can force compensatory hypermetabolism to maintain voltage, distort calcium handling, and disturb neurotransmission timing. At the organism level, that looks like brain fog, dysautonomia, sleep fragmentation, and reduced stress tolerance exactly the systems you don’t want to pay for marginal fat-loss gains. Mechanistically, high-dose signaling also raises the odds of maladaptive redox and substrate partitioning. ERR/PGC-1α drive beta-oxidation and electron delivery to the respiratory chain. If you layer that on top of exercise, fasting, thyroid augmentation, or catecholamine tone, you can overshoot electron influx relative to complex-level throughput, increasing retrograde signaling and forcing the cell to dump potential as heat via uncoupling. At low dose this can be hormetic and helpful. At high dose, it can flatten the ATP/ADP ratio, trigger AMPK hard, suppress mTORC1 anabolics, and blunt hypertrophy. In muscle, that shifts toward more oxidative phenotype at the expense of contractile remodeling; in the heart, it risks energetics imbalance that the sinoatrial node and conduction system must buffer beat-to-beat.