THE GRAND MANIFESTO
Reprogramming the Operating System of Aging & Biological Resilience
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We do not merely observe biology; we engineer its resilience. Operating at the vanguard of systems genetics, microbiome dynamics, and AI-driven multi-omics, our platform rewrites the fundamental code of metabolic and age-related diseases. Moving decisively beyond the limitations of single-target pharmacology, we decipher the systemic cross-talk between host genetics and the gut microbiome. Our mandate is clear: to deliver definitive precision therapeutics—from safeguarding muscle mass in the era of next-generation GLP-1 agonists to neutralizing inflammaging—capturing unparalleled value in the global longevity and metabolic disease markets.
I. The Discovery Engine: Decoding the Gut-Organ Axis for Scalable IP
I. The Discovery Engine: Decoding the Gut-Organ Axis for Scalable IP
Traditional pharmacology suffers from a fundamental blind spot: the systemic architecture of the gut microbiome. We have architected a high-resolution, multi-omics discovery engine—synthesizing transcriptomic, metabolomic, and metagenomic data streams—to map the Gut-Muscle and Gut-Liver axes with unprecedented precision. This engine is not a mere analytical tool; it is a proprietary IP generator. By isolating how specific interventions mechanistically dictate host immunity, muscle protein synthesis, and hepatic lipid metabolism, we continuously harvest novel precision postbiotics and scalable therapeutic assets.
Empirical Validation & IP Foundations: The Discovery Engine
These peer-reviewed milestones serve as our 'Proof of Work'—validating our engine’s capacity to identify and mechanistically prove novel interventions against muscle atrophy and hepatic fibrosis, establishing a formidable economic moat.
Ko, H. et al. (2025) Poncirus trifoliata extract and its active coumarins alleviate dexamethasone-induced skeletal muscle atrophy by regulating protein synthesis, mitochondrial biogenesis, and gut microbiota. Phytotherapy Research. (IF: 6.1, JCR Top 7.2%)
Erdenebileg, S. et al. (2024) Artemisia argyi ethanol extract ameliorates nonalcoholic steatohepatitis-induced liver fibrosis by modulating gut microbiota and hepatic signaling. Journal of Ethnopharmacology. (IF: 5.4, JCR Top 11.9%)
Nguyen, B. N. et al. (2024) Cornflower Extract and Its Active Components Alleviate Dexamethasone-Induced Muscle Wasting by Targeting Cannabinoid Receptors and Modulating Gut Microbiota. Nutrients. (IF: 6.7, JCR Top 16.1%)
II. The Human-Twin In Vivo Architecture: The Ultimate De-risking Sieve
II. The Human-Twin In Vivo Architecture: The Ultimate De-risking Sieve
The primary catalyst for multi-billion-dollar Phase 3 clinical failures is the translational illusion perpetuated by single-genome murine models (e.g., C57BL/6). To eliminate this translational gap, we deploy Diversity Outbred (DO) and Collaborative Cross (CC) cohorts as our definitive 'Human-Twin' architecture. By subjecting massive QTL mapping and epigenetic profiling to human-like genetic variance, we capture the profound gene-by-environment (GxE) interactions that dictate drug efficacy and toxicity. This is not preclinical testing; it is an uncompromising de-risking platform designed to predict and prevent clinical attrition before human trials ever commence.
Empirical Validation & IP Foundations: The Human-Twin Architecture
Demonstrating our platform’s predictive supremacy, these publications confirm that genetic diversity dictates phenotypic response. This is the foundational proof that our DO/CC architecture successfully identifies responder/non-responder dynamics, protecting future clinical investments.
Hong, S., Nguyen, B. N. et al. (2024) Host-specific effects of Eubacterium species on Rg3-mediated osteosarcopenia treatment in a genetically diverse mouse population. Microbiome. (IF: 13.8, JCR Top 4.7% | Highlighted in BRIC & Chosun Biz)
Nguyen, B. N. et al. (2024) Dexamethasone-induced muscle atrophy and bone loss in six genetically diverse collaborative cross founder strains demonstrate phenotypic variability by Rg3 treatment. Journal of Ginseng Research. (IF: 6.8, JCR Top 1.2% - Ranked 1st in field)
Kim, M. et al. (2023) Integrative analysis of hepatic transcriptional profiles reveals genetic regulation of atherosclerosis in hyperlipidemic Diversity Outbred-F1 mice. Scientific Reports. (IF: 5.0)
III. The Zero-Friction Translational Algorithm: Accelerating Bench-to-Market
III. The Zero-Friction Translational Algorithm: Accelerating Bench-to-Market
We operate an AI-native ecosystem where biological intuition is replaced by algorithmic certainty. By integrating our proprietary 'Lab-AGI' intelligence with clinical multi-omics cohorts, we execute a zero-friction translation from preclinical discovery to commercial human application. Whether isolating senescent immune signatures in cancer cachexia or extracting ultra-rare biomarkers from human clinical samples, our algorithmic pipeline ensures that every scientific inquiry is instantly calibrated against critical, high-value unmet medical needs.
Empirical Validation & IP Foundations: The Translational Algorithm
These outputs validate our algorithm’s rapid translational velocity. By bridging preclinical hypotheses with direct clinical relevance—from the gut-immune axis in cancer cachexia to targeted multi-omics interventions—we cement the commercial viability of our pipeline.
Youn, H.Y. et al. (2025) Micheliolide mitigates cancer cachexia through context-dependent modulation of the gut-immune axis. Microbiome. (Accepted | IF: 13.8)
Kang, T. et al. (2025) Anti-Allergic Effects of Chamaecrista nomame Extract and Luteolin in an OVA-Induced Asthma Mouse Model. Phytotherapy Research. (Accepted | IF: 6.1)
Nam, Y. et al. (2023) Sanguisorba officinalis L. ameliorates hepatic steatosis and fibrosis by modulating oxidative stress, fatty acid oxidation, and gut microbiota in CDAHFD-induced mice. Nutrients. (IF: 6.7)
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