Provided herein are methods and compositions relating to glucagon-like peptide-1 receptor (GLP1R) libraries having nucleic acids encoding for a scaffold comprising a GLP1R binding domain. Libraries described herein include variegated libraries comprising nucleic acids each encoding for a predetermined variant of at least one predetermined reference nucleic acid sequence. Further described herein are protein libraries generated when the nucleic acid libraries are translated. Further described herein are cell libraries expressing variegated nucleic acid libraries described herein.

The present invention relates to the discovery of a method for identifying a treatment regimen for a patient diagnosed with cancer, predicting patient resistance to therapeutic agents and identifying new therapeutic agents, obtaining the specificity profile of a therapeutic agent, a method of designing a scaffold of a therapeutic agent directed against a drug-resistant target, drug scaffolds, and methods of uses thereof to identify drugs to treat diseases such as cancer. Specifically, the present invention relates to the use of an algorithm to identify a mutation in a kinase, determine if the mutation is an activation or resistance mutation and then to suggest an appropriate therapeutic regimen. The invention also relates to the use of a pattern matching algorithm and a crystal structure library to predict the functionality of a gene mutation, predict the specificity of small molecule kinase inhibitors and for the identification of new therapeutic agents.

Methods are disclosed herein for detecting a genetic predisposition to focal segmental glomerulosclerosis (FSGS) or hypertensive end-stage kidney disease (ESKD) or both in a human subject, e.g., by detecting the presence of at least one single nucleotide polymorphism (SNP) in an APOL1 gene, such as the C-terminal exon of an APOL1 gene. In a further embodiment, methods are disclosed for detecting resistance of a subject to a disease associated with Trypanosoma infection, e.g., by detecting at least one single nucleotide polymorphism (SNP) in an APOL1 gene, such as the C-terminal exon of an APOL1 gene. Also disclosed are methods for treating a subject infected with T. brucei. The methods include administering a therapeutically effective amount of an APOL1 protein including a S342G substitution, an I384M substitution, and/or a deletion of N388 and Y389 to the subject.

The present invention relates generally methods and kits for detecting binding interactions, in particular protein-protein interactions, and particularly to high throughput methods for labelling, analysing, detecting and measuring protein-protein interactions.

The present invention relates generally methods and kits for detecting binding interactions, in particular protein-protein interactions, and particularly to high throughput methods for labelling, analysing, detecting and measuring protein-protein interactions.

Methods for selecting a binding-element are provided. The method comprised of different steps. A first mixture is formed using at least one target molecule and a plurality of oligomers, followed by incubating the first mixture to form a second mixture comprising at least one target-bound oligomer and at least one target-unbound oligomer. Then a first accelerator is added to cleave the target-unbound oligomer and the target-bound oligomer is separated from the target molecule. This is followed by addition of a second accelerator for ligation, and a third accelerator for amplification followed by sequencing and post sequence analysis to select the binding-element.

Methods for selecting a binding-element are provided. The method comprised of different steps. A first mixture is formed using at least one target molecule and a plurality of oligomers, followed by incubating the first mixture to form a second mixture comprising at least one target-bound oligomer and at least one target-unbound oligomer. Then a first accelerator is added to cleave the target-unbound oligomer and the target-bound oligomer is separated from the target molecule. This is followed by addition of a second accelerator for ligation, and a third accelerator for amplification followed by sequencing and post sequence analysis to select the binding-element.

The present invention relates generally to the field of making novel antigen binding domains against infectious diseases. The present invention also relates to novel CARs that utilize the novel antigen binding domains as an extracellular element. The present invention also relates to use of the novel antigen binding domains as therapeutic agents.

Provided are methods of predicting responsiveness of a subject having an inflammatory bowel disease (IBD) to a tumor necrosis factor (TNF)-alpha inhibitor, by analyzing a frequency of at least one subpopulation of immune cells in a tissue biopsy of the subject. Also provided are methods of selecting a treatment for a subject and kits for determining responsiveness of the subject to treatment with a TNF-alpha inhibitor.

Provided are methods of predicting responsiveness of a subject having an inflammatory bowel disease (IBD) to a tumor necrosis factor (TNF)-alpha inhibitor, by analyzing a frequency of at least one subpopulation of immune cells in a tissue biopsy of the subject. Also provided are methods of selecting a treatment for a subject and kits for determining responsiveness of the subject to treatment with a TNF-alpha inhibitor.