Abstract: Provided herein are non-covalent modifiers of AKT1 of Formula (I), (II), (II-A), (III), (III-A), (III-B), (IV), (IV-A), (IV-B), (V), (V-A), (V-B), (VI), (VI-A), or (VI-B), and pharmaceutical compositions thereof. In some embodiments, the present disclosure provides methods of modulating wild-type AKT1 using a compound or salt of Formula (I), (II), (II-A), (III), (III-A), (III-B), (IV), (IV-A), (IV-B), (V), (V-A), (V-B), (VI), (VI-A), or (VI-B), and pharmaceutical compositions thereof.

Abstract: The present disclosure provides methods and compositions for microglia replacement therapy in a subject in need thereof. In some cases, the method involves administering myeloid cells to the central nervous system of a subject. In some cases, the myeloid cells are derived from embryonic or extraembryonic tissue. In some cases, the myeloid cells are genetically modified. The genetic modification may include a colony stimulating factor 1 receptor (CSF1R) variant that is resistant to a CSF1R inhibitor, yet retains sensitivity to its ligand (e.g., CSF1, IL34).

Abstract: Provided herein are covalent modifiers of AKT1 of Formula (I), (I-A), (II), (II-A), (III), (II-A), or (III-B), and pharmaceutical compositions thereof. In some embodiments, the present disclosure provides methods of modulating AKT1 using a compound or salt of Formula (I), (I-A), (II), (II-A), (III), (III-A), or (III-B), and pharmaceutical compositions thereof.

Abstract: Provided herein are covalent modifiers of AKT1 of Formula (A), (A-1), (I), (I-A), (II), (II-A), (II-B), (III), (III-A), (III-B), (IV), (IV-A), (IV-B), (V), (V-A), (V-B), (VI), (VI-A), (VI-B), (VII), (VII-A), (VII-B), (VIII), (VIII-A), (VIII-B), (IX), (IX-A), (IX-B), (X), (X-A), (X-B), (XI), (XI-A), or (XI-B), and pharmaceutical compositions thereof. In some embodiments, the present disclosure provides methods of modulating AKT1 using a compound or salt of Formula (A), (A-1), (I), (I-A), (II), (II-A), (II-B), (III), (III-A), (III-B), (IV), (IV-A), (IV-B), (V), (V-A), (V-B), (VI), (VI-A), (VI-B), (VII), (VII-A), (VII-B), (VIII), (VIII-A), (VIII-B), (IX), (IX-A), (IX-B), (X), (X-A), (X-B), (XI), (XI-A), or (XI-B), and pharmaceutical compositions thereof.

Abstract: The present disclosure provides methods and compositions for microglia replacement therapy in a subject in need thereof. In some cases, the method involves administering myeloid cells to the central nervous system of a subject. In some cases, the myeloid cells are derived from embryonic or extraembryonic tissue. In some cases, the myeloid cells are genetically modified. The genetic modification may include a colony stimulating factor 1 receptor (CSF1R) variant that is resistant to a CSF1R inhibitor, yet retains sensitivity to its ligand (e.g., CSF1, IL34).

Abstract: Provided herein are covalent modifiers of AKT1 of Formula (I), (I-A), (II), (II-A), (III), (II-A), or (III-B), and pharmaceutical compositions thereof. In some embodiments, the present disclosure provides methods of modulating AKT1 using a compound or salt of Formula (I), (I-A), (II), (II-A), (III), (III-A), or (III-B), and pharmaceutical compositions thereof.

Abstract: Provided herein are non-covalent modifiers of AKT1 of Formula (I), (II), (II-A), (III), (III-A), (III-B), (IV), (IV-A), (IV-B), (V), (V-A), (V-B), (VI), (VI-A), or (VI-B), and pharmaceutical compositions thereof. In some embodiments, the present disclosure provides methods of modulating wild-type AKT1 using a compound or salt of Formula (I), (II), (II-A), (III), (III-A), (III-B), (IV), (IV-A), (IV-B), (V), (V-A), (V-B), (VI), (VI-A), or (VI-B), and pharmaceutical compositions thereof.

Abstract: Described herein are compounds and methods for the modulation of AKT1 proteins, such as AKT1 E17K. In some aspects, the present disclosure provides an AKT1 protein, wherein a compound is bound to a lysine residue of the AKT1 protein. In another aspect, the present disclosure provides compounds of Formula (I) and (II), useful for the modulation of AKT1 proteins. In another aspect, the instant disclosure provides a method of attenuating AKT1 activity using the compounds described herein.

Abstract: EGFR is a frequently overexpressed protein in certain human cancers. Disclosed herein are compositions and methods for the modulation EGFR proteins, specifically EGFR mutants comprising single, double, or triple mutations.

Abstract: The present disclosure provides methods and compositions for microglia replacement therapy in a subject in need thereof. In some cases, the method involves administering myeloid cells to the central nervous system of a subject. In some cases, the myeloid cells are derived from embryonic or extraembryonic tissue. In some cases, the myeloid cells are genetically modified. The genetic modification may include a colony stimulating factor 1 receptor (CSF1R) variant that is resistant to a CSF1R inhibitor, yet retains sensitivity to its ligand (e.g., CSF1, IL34).

Abstract: The disclosure provides conjugates of anti-ASGR1 antibodies or antigen binding fragments thereof to a myeloid cell agonist, compositions comprising the conjugates, and methods of treating liver viral infections with the conjugates. The disclosure also provides for anti-ASGR1 antibodies or antigen binding fragments thereof and methods for using the antibodies or antigen binding fragments thereof in treating liver viral infections.

Abstract: The disclosure provides conjugates of anti-ASGR1 antibodies or antigen binding fragments thereof to a myeloid cell agonist, compositions comprising the conjugates, and methods of treating liver viral infections with the conjugates. The disclosure also provides for anti-ASGR1 antibodies or antigen binding fragments thereof and methods for using the antibodies or antigen binding fragments thereof in treating liver viral infections.

Abstract: Various conjugates and compositions thereof are disclosed for use in the treatment of a liver disease, such as liver cancer and liver fibrosis. The compositions comprise conjugates, wherein the conjugates are comprised of an antibody or antibody construct specific for ASGR1 or ASGR2 attached to a TGF?R1 inhibitor via a linker. Additionally provided are the methods of preparation of the conjugates and compositions thereof.

Abstract: The present invention generally provides methods for B-cell reduction in an individual using CD37-specific binding molecules. In particular, the invention provides methods for B-cell reduction using CD37-specific binding molecules alone, or a combination of CD37-specific binding molecules and CD20-specific binding molecules, in some instances a synergistic combination. The invention further provides materials and methods for treatment of diseases involving aberrant B-cell activity. In addition, the invention provides humanized CD37-specific binding molecules.

Abstract: Electronic files for a localization project may be created and/or managed. The electronic files may be based on a data structure that defines the format and content of the electronic files and may include a first data structure portion that may contain data representing a plurality of references to localization project files. The data structure may includes a second data structure portion that may be associated with the first data structure portion that may contain data that may represent a plurality of references to standard files.

Abstract: The present disclosure provides a humanized anti-CD37 small modular immunopharmaceutical (SMIP) molecule, as well as synergistic combination therapies of CD37-specific binding molecules (such as anti-CD37 SMIP proteins or antibodies) with bifunctional chemotherapeutics (such as bendamustine) that can be administered concurrently or sequentially, for use in treating or preventing B-cell related autoimmune, inflammatory, or hyperproliferative diseases.

Abstract: An embodiment of the present invention includes a technique to calibrate receiver and transmitter in a communication system. N digitized samples I(n) and Q(n) are stored. The N digitized samples represent in-phase and quadrature (I-Q) components, respectively, of a down-converted signal from a receiver. The I-Q components are generated from a quadrature demodulator or modulator having I-Q imbalance. Phase and gain adjustment constants are computed from the N digitized samples to compensate for the I-Q imbalance using a closed form solution. Another embodiment of the present invention includes a technique to calibrate a transceiver in a communication system without using a calibrated reference receiver. A first test signal at a first frequency is injected to a transmitter having a quadrature modulator with I-Q imbalance. The quadrature modulator has a carrier frequency. The transmitter generates a transmitter signal.

Abstract: Immunoglycoproteins, including antibodies, with improved ADCC and altered glycosylation patterns are provided. Also provided are cell culturing methods and media for producing such immunoglycoproteins, and therapeutic uses of such immunoglycoproteins.

Abstract: Creation and management of electronic files for a localization project. The electronic files are based on a data structure that defines the format and content of the electronic files and includes a first data structure portion that contains data that represents a plurality of references to localization project files. Moreover, the data structure includes a second data structure portion that is associated with the first data structure portion that contains data that represents a plurality of references to standard files.

Abstract: The invention relates to novel binding domain-immunoglobulin fusion proteins that feature a binding domain for a cognate structure such as an antigen, a counterreceptor or the like, a wild-type IgG1, IGA or IgE hinge region polypeptide or a mutant IgG1 hinge region polypeptide having either zero, one or two cysteine residues, and immunoglobulin CH2 and CH3 domains, and that are capable of ADCC and/or CDC while occurring predominantly as polypeptides that are compromised in their ability to form disulfide-linked multimers. The fusion proteins can be recombinantly produced at high express levels. Also provided are related compositions and methods, including cell surface forms of the fusion proteins and immunotherapeutic applications of the fusion proteins and of polynucleotides encoding such fusion proteins.