Thiogenesis Therapeutics

Excited to have CEO Dr. Rioux present positive MELAS data at Mitocon 2026 - proof of concept, biomarkers and early efficacy signals. $TTI.v $TTIPF #MELAS #Mitocon newsfilecorp.com/release/281290…

Good post - lets add inherited mitochondrial disease and fatty liver disease to the list. $TTI.v $TTIPF #MELAS #Leighs #pedMASH #oxidativestress

Amen! $TTI.v $TTIPF #mito #MELAS #Leigh #oxidativestress

Looking forward to it. $TTI.v $TTIPF #glutathione #taurine #cysteine #oxidativestress #mito

Taurine improves literally every metric of insulin resistance. New review, finding taurine supplementation: ↓ Fasting blood glucose: −5.90 mg/dL ↓ HbA1c: −0.21% ↓ Fasting insulin: ~10-20% ↓ HOMA-IR: −0.57 ↓ Triglycerides: −14.42 mg/dL ↓ Total cholesterol: −12.41 mg/dL ↓ LDL-C: −5.08 mg/dL ↓ Systolic BP: −4.38 mmHg ↓ Diastolic BP: −2.54 mmHg ↓ AST: −9.65 U/L ↓ ALT: −8.26 U/L ↓ CRP: 2-5 mg/L ↓ TNF-α: −0.35 pg/mL Below I cover its protective mechanisms, other benefits and how to get enough in food + supps.

Inflammation is behind nearly every chronic disease— From stubborn belly fat to heart attacks. But no one talks about how to actually fix it. Here are 10 underrated anti-inflammatory cheat codes your doctor won't mention:🧵

TTI-0102 is a precursor to hypotaurine which is oxidized into Taurine -- excellent summary below $TTI.v $TTIPF #taurine #mitochondria #MELAS #Leighsyndrome

The beauty of taurine beyond everything mentioned here is the fact that it has a sparing effect on nutrients tied to methylation (especially when saturated with all methylation nutrients) due to cysteine's metabolism down the transsulfuration pathway. This means higher doses of taurine can not only spare magnesium—GABA—inhibitory effects in the central nervous system, but also spare small amounts of glutathione, methionine, choline/betaine, vitamin B2/B3/B9/B12, and glycine. Not to mention that taurine is also greatly connected to supporting mitochondrial function and redox support. Thus, having an even further effect on this pathway.

Nice post about mitochondrial health - well worth a read.

Eager to add a Phase 3 orphan program to the company's pipeline. $TTI.v $TTIPF #cystinosis #lysosome #orphandrug newsfilecorp.com/release/275563…

Exciting news - interim phase 2 MELAS data, update on Leigh syndrome $ the introduction of a new late stage clinical program in cystinosis! $TTI.v $TTIPF #MELAS #cystionsis newsfilecorp.com/release/273012…

Please to provide corporate update on AGM and 2025 - $TTI, $TTIPF, #mito, #MELAS, #Leigh, #MASH newsfilecorp.com/release/265967…

@FierceBiotech Hopeful - would be great for the the Barth's patients to have options, when they have little now. #mito #mitodisease #curemito

The FDA has accepted Stealth BioTherapeutics’ third new drug application for its ultrarare disease candidate, providing a planned decision date of Sept. 26. fiercebiotech.com/biotech/fda-ac…

The ORPHAN Cures Act will enable more options for Americans living with rare disease. Congress must pass the #ORPHANCuresAct to ensure continued investment in lifesaving treatments and to protect U.S. #biotech leadership.

@MarcosArrut Can you do telomeres next?

Is Aging caused by DNA damage? No. And I’ll explain why. In a previous post, I explained why mitochondrial damage does not cause aging. Now it's DNA damage's turn. For decades, one of the most accepted theories held that aging was the result of accumulated damage to DNA. This idea, born after Watson and Crick’s discovery of the double helix, seemed intuitive: if DNA contains the instructions to build and maintain the organism, then the deterioration of those instructions should lead to the progressive collapse of the biological system. In theory, it made sense. In practice, it doesn't. Today we know that this explanation is imprecise and, in many ways, outdated. First, only 2% of the human genome is coding. The remaining 98% corresponds to non-coding regions. While there are regulatory elements in those non-coding regions (such as microRNA zones), there are also large amounts of sequences that are functionally dispensable—or even useless. Now, if aging were caused by random DNA damage, we would expect to observe a chaotic and asymmetric phenomenon across cells and tissues, since not all cells would be damaged in the same way or at the same time. However, what we actually see is the opposite: aging is surprisingly homogeneous, synchronous, and predictable. The cells of a given tissue age in a coordinated fashion, as if obeying a common program. The odds of all cells accumulating the same damage, in the same DNA regions, at the same time, across the same tissues and species, are zero. Chance does not orchestrate symphonies. This brings us to a fundamental distinction: not all DNA damage carries the same biological meaning. Cancer, for example, is caused by mutations. But cancer and aging are completely different phenomena. Cancer arises from a single cell with mutations. Aging, on the other hand, is a systemic process: all cells in the body participate, and they do so in an orderly way, following specific temporal patterns that are even conserved across species. It’s also true that if we deliberately damage an organism's DNA, we can accelerate its deterioration. But that doesn’t mean DNA damage is the natural cause of aging. Let me explain it simply: Think of a smartphone with a built-in programmed obsolescence system. If we throw it into water, it will start malfunctioning prematurely. But not because the water accelerated the obsolescence program, or because the water is that program. We simply added entropy. In the same way, damaging DNA introduces entropy into a system that already had its own internal biological clock. It would age anyway—only now it does so under worse conditions. Aging does not require that external entropy to occur. It’s already programmed to happen, even in organisms kept under optimal conditions. In an aged organism, we observe DNA damage, but that damage is a consequence of aging—not its cause. The same goes for mitochondrial dysfunction, loss of proteostasis, or even epigenetic damage (we'll talk about this in a future post)—all of these are symptoms of the process, not its engine. The key is to understand that aging is not biological entropy. It is an active, regulated, genetically programmed process. It’s not disorder. It’s the architecture of decline. And that detail is not minor. It gives us a strong clue about how we should act. We must intervene in the biological algorithm that activates decline. We must turn off the aging genes, restore youthful epigenetics, and reset the cellular timeline. That's not futurism. It's engineering. And we're heading straight for it. That's all.

Looking forward to filing IMPD for a Ph 2a pediatric MASH trial in the EU - an unserved market for kids with severe liver disease. $TTIV $TTIPF #mito #fattyliver #oxidativestress newsfilecorp.com/release/256736…

Looking forward to a good turnout at MitoMed 2025. $TTI.v $TTIPF #mito #Leigh's #melas newsfilecorp.com/release/256143…

Thiogenesis is excited to start dosing MELAS patients in France, looking forward to interim data in September. $TTI.v $TTIPF #mito #MELAS #Angers newsfilecorp.com/release/255687…

Great news today - excited to clear IND for LSS. $TTI.v $TTIPF #mitochondria #Leighsyndrome #cysteine #glutathione #IND newsfilecorp.com/release/255101…