Loading patent…
AssigneeHeptares Therapeutics Limited
InventorsMalcolm Peter Weir, Richard Henderson, Christopher Gordon Tate, Francesca Magnani, Maria Josefa Serrano-Vega, Yoko Shibata, Antony Johannes Warne
Estimating the term…
A method of producing a conformational specific binding partner of a GPCR, the method comprising: a) providing a mutant GPCR of a parent GPCR, wherein the mutant GPCR has increased stability in a particular conformation relative to the parent GPCR; b) providing a test compound; c) determining whether the test compound binds to the mutant GPCR when residing in a particular conformation; and d) isolating a test compound that binds to the mutant GPCR when residing in the particular formation. Methods of producing GPCRs with increased stability relative to a parent GPCR are also disclosed.
1-108. (canceled)
A mutant human G-protein coupled receptor (GPCR) with increased conformational stability in a particular conformation compared to its parent human GPCR in the same particular conformation.
A mutant human G-protein coupled receptor (GPCR) with increased conformational stability compared to its parent GPCR, which mutant GPCR has an extended lifetime of a particular conformation relative to the same conformation of its parent GPCR under denaturing conditions, the extended lifetime being manifest by retention of ligand binding ability.
A mutant G-protein coupled receptor (GPCR) with increased conformational stability in a particular conformation compared to its parent GPCR in the same particular conformation, and wherein the mutant is not a mutant rat neurotensin receptor, which, when compared to its parent rat neurotensin receptor, contains an F358A mutation according to the numbering of the rat neurotensin receptor as set forth in SEQ ID NO:
A mutant G-protein coupled receptor (GPCR) with increased conformational stability compared to its parent GPCR which mutant PCR has an extended lifetime of a particular conformation relative to the same conformation of its parent GPCR under denaturing conditions, the extended lifetime being manifest by retention of ligand binding ability, and wherein the mutant is not a mutant rat neurotensin receptor, which, when compared to its parent rat neurotensin receptor, contains an F358A mutation according to the numbering of the rat neurotensin receptor as set forth in SEQ ID NO:
Dependencies are inferred from the claim text.