Jnana Therapeutics Inc. has described sodium-dependent neutral amino acid transporter B(0)AT1 (SLC6A19) inhibitors reported to be useful for the treatment of diabetes, chronic kidney disease, nonalcoholic or metabolic dysfunction-associated steatohepatitis (NASH/MASH), phenylketonuria, metabolic syndrome, obesity, neurodevelopmental disorders and autism spectrum disorders, among others.
Tokyo-headquartered Otsuka Pharmaceutical Co. Ltd. said Aug. 1 that it will acquire Boston-based Jnana Therapeutics Inc. through a potential $1.125 billion M&A deal. Under the terms, Otsuka will work to close the transaction by the third quarter of 2024, with $800 million paid out to Jnana shareholders, along with up to $325 million in additional development and regulatory milestones payments.
Tokyo-headquartered Otsuka Pharmaceutical Co. Ltd. said Aug. 1 that it will acquire Boston-based Jnana Therapeutics Inc. through a potential $1.125 billion M&A deal. Under the terms, Otsuka will work to close the transaction by the third quarter of 2024, with $800 million paid out to Jnana shareholders, along with up to $325 million in additional development and regulatory milestones payments.
Jnana Therapeutics Inc. has synthesized sodium-dependent neutral amino acid transporter B(0)AT1 (SLC6A19) inhibitors reported to be useful for the treatment of amino acid metabolism disorders, amino acid transport disorders and metabolic and nutritional genetic disorders, among others.
Jnana Therapeutics Inc. has identified sodium-dependent neutral amino acid transporter B(0)AT1 (SLC6A19) inhibitors reported to be useful for the treatment of diabetes, chronic kidney disease, metabolic dysfunction-associated steatohepatitis, phenylketonuria, metabolic syndrome, obesity, neurodevelopmental and autism spectrum disorders, among others.
Work at Jnana Therapeutics Inc. has led to the identification of sodium-dependent neutral amino acid transporter B(0)AT1 (SLC6A19) inhibitors reported to be useful for the treatment of diabetes, chronic kidney disease, metabolic dysfunction-associated steatohepatitis (MASH), phenylketonuria, metabolic syndrome, obesity, neurodevelopmental and autism spectrum disorders, among others.
Phenylketonuria (PKU) is an inborn error of metabolism caused by heritable phenylalanine hydroxylase gene mutations that result in decreased metabolism of phenylalanine (Phe) causing brain damage. The most severe phenotype termed PKU occurs when untreated individuals achieve plasma Phe concentrations of >1200 microM/L, which are neurotoxic.
Phenylketonuria (PKU) is an autosomal recessive disorder where the primary catabolic pathway for phenylalanine (Phe) is disrupted due to mutations in the gene encoding PAH. Elevated Phe levels lie behind several neuropathologic anomalies that can lead to severe and irreversible mental retardation, if untreated.
Belharra Therapeutics Inc., an early stage firm which is pioneering a new approach to chemoproteomics, has already found an influential backer for the distinctive way it systematically probes the interactions between small-molecule ligands and the proteins to which they bind.
Momentum is building at Jnana Therapeutics Inc. The firm has raised $107 million in a series C round and banked another $50 million up front from a new drug discovery and development pact with Roche Holding AG, which could potentially deliver significant near-term milestones and more than $2 billion in future milestone payments. It also commenced recruitment onto a first-in-human study of its lead drug candidate, JNT-517, an inhibitor of the phenylalanine transporter SLC6A19, which is in development for phenylketonuria.
