40 results about "Colony-stimulating factor" patented technology

The application discloses a use of Ejiao Qianggu oral liquid in regulating immunity, and particularly relates to an improving effect of the Ejiao Qianggu oral liquid on an immune system, which is realized by the following aspects. On one hand, the Ejiao Qianggu oral liquid promotes proliferation and transformation (mainly early T lymphocytes and part of B lymphocytes) and active functions of spleen lymphocytes; on the other hand, the Ejiao Qianggu oral liquid improves phagocytosis of macrophages. The Ejiao Qianggu oral liquid has the following characteristics: firstly, the Ejiao Qianggu oral liquid acts on early lymphocyte maturation, and has no significant effect on proliferation of peripheral blood lymphocytes; secondly, the Ejiao Qianggu oral liquid can significantly act on immune target organs, thymus and spleen tissues, and does not excessively stimulate the spleen, unlike positive drugs such as colony stimulating factor which can cause significant edema of the spleen; and thirdly, the Ejiao Qianggu oral liquid has a significant recovery effect on body weight, white blood cells, lymphocytes, red blood cells and hemoglobin in blood of patients with low immunity.

The present disclosure relates to a method for reducing or hindering development of renal ischemia-reperfusion injury in a subject the method comprising administering an antibody that inhibits granulocyte colony stimulating factor (G-CSF) signaling. In some examples, the ischemia-reperfusion injury is due to or associated with tissue or organ transplantation.

The present invention relates to a method of producing macrophages. The macrophages are produced from monocytes harvested from a subject by incubating said monocytes in a medium comprising a Colony Stimulating Factor 1 Receptor (CSF-1R) agonist. Before monocytes are harvested, the subject is treated with G-CSF. The macrophages produced by the method are capable of being polarised to a pro-restorative, anti-inflammatory and / or anti-fibrotic phenotype. The invention also relates to methods of treating inflammatory diseases comprising administering the macrophages produced by the method to a subject.

The application provides a hyaluronic acid artificial lymph node sustained-release nano DNA vaccine for enhancing cancer prevention effect and a preparation method thereof, and the preparation raw materials comprise a plasmid, 4-(bromomethyl)phenyl boronic acid modified linear polyethylene imine, a cell colony stimulating factor, a sulfhydryl modified hyaluronic acid and a four-arm-maleimide grafted polyethylene glycol. The nano DNA vaccine can recruit a large number of immune cells to form a hyaluronic acid artificial lymph node after subcutaneous administration, and inhibit the generation of tumors by continuously outputting antigen presenting cells and antigen specific T cells. In addition, the hyaluronic acid artificial lymph node can also release the nano DNA vaccine, prolong the vaccine stimulation time, improve the problem of weak immunogenicity of the existing DNA vaccine, and also solve the problem of biocompatibility. The nano DNA vaccine has the advantages of easy preparation, easy storage, low price and the like.

Disclosed is a method of impeding platinum-based chemotherapeutic induced ototoxicity, and / or other toxicity, the method comprising administering a colony stimulating factor 1 receptor (CSF1R) inhibitor to a subject in an amount sufficient to impede ototoxicity, and / or other toxicity, inducible by a platinum-based chemotherapeutic; and administering the platinum-based chemotherapeutic to the subject. The CSF1R inhibitor can be, for example, pexidartinib. The platinum-based chemotherapeutic can be, for example, cisplatin. Compositions, medicaments, kits, and uses are disclosed related to the same. Further, a method of screening for a compound able to impede a platinum-based chemotherapeutic induced toxicity is disclosed.

The present invention discloses a recombinant nucleic acid molecule encoded by at least ORF (100, 100a) to reduce cytokine storm during immunotherapy. The recombinant nucleic acid molecule comprises at least one first hairpin ring structure, at least one second hairpin ring structure and a first promoter (120). The first hairpin loop structure is formed from one or more first short hairpin RNA (130a) sequences. The first hairpin ring structure modulates the amount of interleukin 6 (IL6) cytokine during immunotherapy. The second hairpin loop structure is formed from one or more second short hairpin RNA (130b) sequences. The second hairpin ring structure modulates the amount of granulocyte monocyte colony stimulating factor (GMCSF) cytokine during immunotherapy and is disposed upstream or downstream of the first hairpin ring structure. The first promoter (120) is disposed upstream of the first hairpin ring structure and the second hairpin ring structure.

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.

The present invention relates to a treatment regime, including an antibody or antigen-binding fragment which is capable of binding specifically to colony stimulating factor-1 receptor (CSF-1R) for use in the treatment of tenosynovial giant cell tumour (TGCT) in a subject, as well as associated uses and methods.

The present disclosure provides methods of treating chronic graft versus host disease (cGVHD) using antibodies that bind to colony stimulating factor 1 receptor (CSF-1R).

The present disclosure describes a combination of an anti-colony stimulating factor 1 receptor antibody and a JAK inhibitor for the treatment of chronic graft-versus-host disease.

The present invention provides a method of treating a disease or disorder caused by and / or associated with CSF1R dysfunction in a human patient, the method comprising administering to the patient in need thereof an effective amount of a compound that increases the activity of triggering receptor expressed on myeloid cells 2 (TREM2). In some embodiments, compound that increases the activity of TREM2 is an agonist of TREM2. In some embodiments, the agonist of TREM2 is a small molecule agonist of TREM2 or an antibody agonist of TREM2.

The invention relates to the field of neurology, neurobiology, and neurological disorders. The invention relates to a pharmaceutical combination comprising a colony-stimulating factor 1 receptor (CSFR1R) inhibitor and a bone marrow cell population for use in the treatment of central nervous system (CNS) diseases. The invention further relates to an ex vivo method for depleting dysfunctional and / or mutant microglia and / or CNS-associated macrophages (CAM), the method comprising providing a population of cells comprising myeloid cells and treating said cells with an CSF1R inhibitor of central nervous system (CNS)-associated myeloid cells, thereby depleting dysfunctional and / or mutant microglia. The invention relates to a cell population according to the ex vivo method. The invention further relates to a pharmaceutical composition comprising the CSF1R inhibitor according to the present invention for use in the treatment or prevention of a medical condition induced by dysfunction of immune cells in a central nervous system (CNS), additionally comprising a pharmaceutically acceptable carrier.

The invention provides application of a neutralizing antibody of a targeted macrophage to preparation of a medicine for treating atopic dermatitis (AD), relates to the technical field of biomedicine, and is characterized in that the neutralizing antibody of the targeted macrophage is provided to deplete the macrophage so as to treat the AD. The method is characterized in that a neutralizing antibody capable of specifically recognizing and combining a key target spot-colony stimulating factor 1 receptor (CSF1R) on the surface of the macrophage is applied to block a CSF1 / CSF1R signal channel, so that the macrophage for driving the AD pathological process is eliminated. According to the application, the atopic dermatitis (AD) is treated by applying the neutralizing antibody targeting the key target spot of the macrophage, and remarkable and multi-aspect beneficial technical effects are generated. The effects are verified in an AD mouse model induced by MC903 and are specifically reflected in relieving of disease core symptoms, intervention of key pathological links and improvement of overall health conditions, and a foundation is laid for clinical treatment of atopic dermatitis.

Colony Stimulating Factor, CSF, refers to a family of four glycoproteins that control and coordinate cell production by widely scattered deposits of marrow cells. GM-CSF is a hematologic growth factor that regulates the production, migration, proliferation, differentiation and function of hematopoietic cells. The present disclosure relates generally to compositions and methods related to long acting and granulocyte-macrophage colony-stimulating factor (GM-CSF) with improved pharmacokinetics.

Disclosed are single chain polypeptides exhibiting both Interleukin-10 (IL-10) and Colony-Stimulating Factor 1 (CSF1) activities. The polypeptides are engineered to selectively deliver the anti-inflammatory effects of IL-10 to myeloid cells that express the CSF1 receptor (CSF1R). In one embodiment, the polypeptide comprises a CSF1 monomer fused via a peptide linker to an IL-10 monomer. In another embodiment, the polypeptide comprises a single chain dimeric IL-10 fused to a CSF1 monomer. These fusion proteins provide targeted anti-inflammatory activity while reducing systemic effects on other immune cells. Pharmaceutical compositions containing these polypeptides and their use for treating inflammatory diseases, such as inflammatory bowel disease, are also provided.

The application discloses a preparation method of a composition for ovary transplantation and the composition. The composition comprises an antioxidant peptide and a colony stimulating factor. The antioxidant peptide in the composition of the application is attached to the colony stimulating factor, so that the antioxidant peptide can reach a ROS site, the antioxidant peptide can remove active oxygen generated by the ROS site and weaken the oxygen generation capacity of the ROS site, the antioxidant effect is improved, follicle loss is reduced, more follicles are protected, and finally the effect of frozen-thawed ovary tissue transplantation is improved.

Compounds of the formulaor pharmaceutically acceptable salts thereof, and pharmaceutical compositions comprising the same. The compounds are useful as colony stimulating factor-1 receptor inhibitors (“CSF-1R inhibitors”).

The present disclosure provides, among other things, anti-CSF1R single-domain antibodies (sdAbs) with high affinity to CSF1R (e.g., KD of pM to low nM) and therapeutic uses of such sdAbs in effectively treating CSF1R mediated diseases, such as age-related macular degeneration (AMD). In some embodiments, an anti-CSF1R sdAb is fused to an Fc region.

The invention relates to a composition and application of the composition in preparation of drugs for treating Alzheimer's disease, the composition comprises hematopoietic stem cells modified by an adenine base editing system and a colony stimulating factor 1 receptor inhibitor, the use method of the medicine for treating the Alzheimer disease comprises the following steps: S1, using the colony stimulating factor 1 receptor inhibitor to deplete microglial cells in the brain; s2, performing marrow removal pretreatment; s3, transplanting the hematopoietic stem cells modified by an adenine base editing system, wherein the adenine base editing system is used for correcting R47H site mutation of the TREM2 gene in the hematopoietic stem cells; experiments prove that when the base editing system and the CSF1 inhibitor are combined for use, microglial cells in the brain can be replaced, A beta load in the brain can be reduced, neuroinflammation can be relieved, cognitive impairment can be improved, the effect is remarkably superior to that of a single therapy, and an unprecedented comprehensive treatment scheme is provided for solving systematic immunodeficiency of the Alzheimer disease.

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.

The present disclosure describes a combination of an anti-colony stimulating factor 1 receptor antibody and a JAK inhibitor for the treatment of chronic graft-versus-host disease.

The present invention is directed to a method for producing granulocytes and / or precursors thereof for therapeutic use, the method comprising culturing progenitor cells in a cell culture medium comprising: (a) an inhibitor of p38 MAP kinase; (b) granulocyte macrophage-colony stimulating factor (GM-CSF); and (c) interleukin-3 (IL-3). Also provided are a granulocyte and / or precursor thereof, population of cells, composition, kit, and therapeutic uses thereof.

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.

Mammals typically heal with fibrotic scars. Treatments to regenerate human skin and hair without a scar remain elusive. Mice lacking C-X-C motif chemokine receptor 2 (CXCR2-KO) displayed robust and complete tissue regeneration across three different injury models, including skin, hair follicle, and cartilage. Remarkably, wild type mice receiving plasma from CXCR2-KO mice through parabiosis or injections healed wounds scarlessly. A comparison of circulating proteins using multiplex ELISA revealed a 24-fold higher plasma level of granulocyte-colony stimulation factor (G-CSF) in CXCR2-KO blood. Local injections of G-CSF into WT mouse wound beds reduced scar formation and increased hair follicle regeneration by 6-fold. G-CSF directly polarized macrophages into an anti-inflammatory phenotype, and both CXCR2-KO and G-CSF-treated mice recruited more anti-inflammatory macrophages into injured areas. These results improve our molecular understanding of scarless tissue regeneration and introduce a new therapeutic approach for cutaneous wounds and hair regeneration. Provided are compositions and methods relating to treating wound healing pathologies.

The present invention relates to a monoclonal antibody, or fragment thereof, which binds to CSF-1R (Colony stimulating factor 1 receptor), in particular to human CSF-1R. The present invention further relates to the in vitro use of the monoclonal antibody, or fragment thereof, of the present invention for the detection of CSF-1R in a sample. Further encompassed by the present invention is a complex comprising the monoclonal antibody, or fragment thereof, of the present invention and CSF-1R such as the human CSF-1R polypeptide.

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).

The present disclosure provides methods of treating chronic graft versus host disease (cGVHD) associated obliterated bronchiolitis syndrome using antibodies that bind to colony stimulating factor 1 receptor (CSF-1R).

The present invention discloses a recombinant nucleic acid molecule encoded by at least ORF (100, 100a) to reduce cytokine storm during immunotherapy. The recombinant nucleic acid molecule comprises at least one first hairpin ring structure, at least one second hairpin ring structure and a first promoter (120). The first and second hairpin ring structures modulate the amount of granulocyte monocyte colony stimulating factor (GMCSF) cytokine and interleukin 6 (IL6) cytokine, respectively. The first hairpin ring structure is formed from at least two first short hairpin RNA (130a) sequences and at least one microRNA30 (130) sequence. The second hairpin ring structure is formed from at least two second short hairpin RNA (130b) sequences and at least one microRNA30 (130) sequence. The first promoter (120) is disposed upstream of the first and second hairpin ring structures.