METHODS OF TREATMENT USING G-CSF PROTEIN COMPLEX

    公开(公告)号:US20230027238A1

    公开(公告)日:2023-01-26

    申请号:US17781639

    申请日:2020-12-04

    摘要: This disclosure provides a method of preventing, alleviating or treating a condition (i.e., neutropenia) in a subject in need thereof, the condition characterized by compromised white blood cell production in the subject. The method includes administering to the subject a therapeutically effective amount of a protein complex on the same day as a chemotherapy regimen, wherein the protein complex is a modified human granulocyte-colony stimulating factor (hG-CSF) covalently linked to an immunoglobulin Fc region via a non-peptidyl polymer. The non-peptidyl polymer is site-specifically linked to an N-terminus of the immunoglobulin Fc region, and the modified hG-CSF comprises substitutions in at least one of Cys17 and Pro65.

    CHIMERIC ANTIGEN RECEPTOR T CELL THERAPY

    公开(公告)号:US20220378830A1

    公开(公告)日:2022-12-01

    申请号:US17743288

    申请日:2022-05-12

    申请人: Kite Pharma, Inc.

    摘要: The disclosure provides methods of treating a malignancy comprising administering an effective dose of an immune cell therapy (e.g., a chimeric antigen receptor genetically modified T cell immunotherapy) and methods for manufacturing such immunotherapy. Some aspects of the disclosure relate to methods of determining objective response of a patient to an immune cell immunotherapy based on the levels of patient and product attributes prior to and after administration of the immunotherapy to the patient.

    Compositions and methods for inhibiting tumor-induced immune suppression

    公开(公告)号:US11446352B2

    公开(公告)日:2022-09-20

    申请号:US16180203

    申请日:2018-11-05

    发明人: Ahmed Chadli

    摘要: It has been discovered that the cyclic peptide EnnA inactivates the Hsp90 chaperone pathway, but without activating an extensive heat shock response and overexpression of anti-apoptotic proteins. Mechanistically distinct, EnnA inhibits Hsp90 and destabilize PDL-1 and IDO, two major immune checkpoints mediating tumor-induced immune suppression. The provided herein show that EnnA profoundly modulates the cytokine signature of cancer cells and promotes a cytokine profile that favors an immune attack on tumor cells. This translates into highly efficacious anti-tumor activity in vivo, which, when combined with a single dose of chemotherapy, completely reduced the tumor burden in experimental animals and instilled highly efficient immune memory against the primary tumor.