ArticleCell host & microbe2024
The live biotherapeutic SYNB1353 decreases plasma methionine via directed degradation in animal models and healthy volunteers.
Article in Cell host & microbe, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Spatiotemporal dynamics of the host-tumor metabolic interface: Implications for precision nutritional oncology.Genes & diseases · 2026Review
- Engineering commensal microbes for host health.Cell host & microbe · 2026Review
- Methionine restriction and mimetics to ameliorate human aging and disease.Trends in endocrinology and metabolism: TEM · 2026Review
- An orally administrable hydrogen-bonded organic framework (HOF)-based nanoreactor to reprogram metabolism for senescence intervention.National science review · 2026Article
- Translational approaches in microbiome research: from functional mechanisms to next-generation therapeutics.Frontiers in microbiology · 2026Review
- Homocystinuria: Advances in metabolic and molecular therapies targeting homocysteine pathways (Review).Molecular medicine reports · 2026Review
- Engineered bacteria: a novel era for metabolic, cardiovascular and cerebrovascular diseases therapy.Frontiers in cardiovascular medicine · 2026Review
- Recent Insights About Probiotics Related Pharmabiotics in Pharmacology: Prevention and Management of Diseases.Probiotics and antimicrobial proteins · 2025Review
- Methionine Dependency and Restriction in Cancer: Exploring the Pathogenic Function and Therapeutic Potential.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The Future of Microbiome Therapeutics.Drugs · 2025Review
- Next-generation probiotics and engineered BEVs for precision therapeutics in osteoporosis.Frontiers in nutrition · 2025Review
- Bacterial live therapeutics for human diseases.Molecular systems biology · 2024Review
- Living Engineered Bacterial Therapeutics: Emerging Affordable Precision Interventions.Microbial biotechnology · 2024Review
- Diagnosing and engineering gut microbiomes.EMBO molecular medicine · 2024Review
- Article
- Conquering homocystinuria with engineered probiotics.Cell host & microbe · 2024Article
- A Phase I Trial of a Methionine Restricted Diet with Concurrent Radiation Therapy.Nutrition and cancer · 2024Article
- Muscarinic receptor drug trihexyphenidyl can alter growth of mesenchymal glioblastomaFrontiers in pharmacology · 2024Article
- Empowering probiotics with high xanthine transport for effective hyperuricemia management.Gut microbesArticle
- Engineered Methioninase-expressing Tumor-targetingCancer genomics & proteomicsArticle
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18 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methionine is an essential proteinogenic amino acid, but its excess can lead to deleterious effects. Inborn errors of methionine metabolism resulting from loss of function in cystathionine β-synthase (CBS) cause classic homocystinuria (HCU), which is managed by a methionine-restricted diet. Synthetic biotics are gastrointestinal tract-targeted live biotherapeutics that can be engineered to replicate the benefits of dietary restriction. In this study, we assess whether SYNB1353, an E. coli Nissle 1917 derivative, impacts circulating methionine and homocysteine levels in animals and healthy volunteers. In both mice and nonhuman primates (NHPs), SYNB1353 blunts the appearance of plasma methionine and plasma homocysteine in response to an oral methionine load. A phase 1 clinical study conducted in healthy volunteers subjected to an oral methionine challenge demonstrates that SYNB1353 is well tolerated and blunts plasma methionine by 26%. Overall, SYNB1353 represents a promising approach for methionine reduction with potential utility for the treatment of HCU.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.