15 results about "EGFR binding" patented technology

Provided are a B7-H3 binding molecule, an EGFR binding molecule, a B7-H3 / EGFR binding molecule, methods for treating cancers by using the binding molecules, and related pharmaceutical uses thereof.

The invention discloses a compound of a Galectin-3 and EGFR (Epidermal Growth Factor Receptor) double-target inhibitor in the technical field of biological medicines, and the compound disclosed by the invention not only shows a relatively strong Galectin-3 and EGFR binding effect, but also has certain in-vitro anti-hepatic fibrosis activity, and can be applied to Galectin-3 and EGFR target related tumor diseases. As a double-target anti-hepatic fibrosis candidate compound based on Galectin-3 and EGFR, which is reported for the first time, the compound has further values of research and development and research of original new drugs based on double targets of Galectin-3 and EGFR.

Provided herein are engineered IgA antibodies that comprises: (a) an EGFR binding domain and (b) an IgA heavy chain constant region. Also, provided herein are methods of treating cancer in a subject in need thereof, the method comprising administering to the subject an effective amount of the engineered antibody.

The disclosure relates to means and methods for administration of antibodies in the treatment of cancer. The disclosure in particular relates to a method of reducing infusion-related reactions in the treatment of a cancer in an individual with an EGER binding and / or complement activating antibody.

A binding domain having a binding specificty to human EGFR (epithelium growth factor receptor) comprises a VH domain and a VL domain, wherein the VH and VL domain each independently comprises a sequence having at least 90% sequence identify to an amino acid sequence as disclosed thereof. The application further provides antibodies comprising the binding domain.

The invention discloses a protein degradation targeting chimera for an EGFR-VHL system. The protein degradation targeting chimera comprises an EGFR binding molecule and a VHL binding molecule, the EGFR binding molecule is any one of proteins as shown in SEQ ID NO.1 to SEQ ID NO.3; the VHL binding molecule is any one of proteins as shown in SEQ ID NO. 4 to 37. The invention also discloses application of the protein degradation targeting chimera in preparation of drugs targeting EGFR and VHL. The invention provides a set of complete calculation design framework, a diversified candidate binding protein library is generated, and finally three high-quality EGFR binding proteins and 34 high-quality VHL binding proteins are obtained and show excellent prediction evaluation indexes. The invention establishes a general framework which is preliminarily verified and is suitable for the rational design of the next generation of protein PROTAC, and lays a foundation for a targeted protein degradation treatment strategy of tumors and other diseases.

Bispecific antibody against EGFR and c-Met. The heterodimeric interaction between the EGFR binding arm and the c-Met binding arm of the bispecific antibody is stronger than the interaction of each in the source homodimer by modifying the Fc segment amino acid sequence of the binding arm, so that it can be assembled into a heterodimer in vitro; its effect on inhibiting the proliferation of EGFR and c-Met double-positive tumor cells is stronger than the combination of EGFR monoclonal antibody and c-Met monoclonal antibody, mediates antibody-dependent cellular cytotoxicity (ADCC), promotes target protein internalization and inhibits the proliferation of osimertinib acquired resistant cell lines. Since the prepared bispecific antibody is simple to prepare, stable in structure, and can obtain a pure bispecific antibody by in vitro assembly, it is expected to better meet the clinical treatment needs, and therefore has a good market prospect.

Disclosed are bispecific antibodies against EGFR and MET. The amino acid sequence of the Fc segment of the binding arm is modified, so that a KIH structure is formed between the EGFR binding arm and the cMet binding arm of the bispecific antibody, and a heterodimer is assembled; the ADCC activity of the bispecific antibody is enhanced, or the inhibition intensity of ligand-mediated antigen phosphorylation is enhanced. The prepared bispecific antibody is simple to prepare and stable in structure, and has a better tumor inhibition effect, so that the bispecific antibody has a good market prospect.

Provided herein is an engineered IgA antibody comprising: (a) an EGFR binding domain and (b) an IgA heavy chain constant region. Further provided herein is a method of treating a cancer in a subject in need thereof, the method comprising administering to the subject an effective amount of the engineered antibody.

The present invention relates to antigen binding proteins that bind to ligand binding sites of EGFR and to clinically related EGFR escape mutations. Specifically, the present invention provides antigen binding proteins comprising a first antibody variable domain and a second antibody variable domain wherein the variable domains form a binding site that specifically binds to human epidermal growth factor receptor (EGFR) variants having one or more of mutated V441D, S464L, G465R and S492R, and that specifically bind to human epidermal growth factor receptor (EGFR) variants having one or more of mutated V441D, S464L, G465R and S492R, determining the bound KDlt by biolayer interferometry (BLI); 10 to 5 moles; and which does not bind to human EGFR having the mutation Q435P and / or the double mutation F436A / I462A, the bound KDgt being determined by biolayer interferometry (BLI); and 10 to 5 moles. The binding of the antigen binding protein to the human EGFR blocks the activation of the human EGFR induced by the ligand.

A method of treating a patient suffering from a cancer driven by a dysregulated human epidermal growth factor receptor (HER1 / human EGFR) comprising administering to a patient in need of such treatment a flexible proactive regimen to combine an anaplastic lymphoma kinase inhibitor (ALK inhibitor) with an anti-EGF antibody (mAb) for inhibiting the pathway activated by EGF-EGFR binding. The anti-EGF antibody can be produced by proactive immunization or provided passively by administration of an anti-EGF antibody. The method comprises administering the ALK inhibitor according to a continuous regimen based on an average daily dose ranging from 10 to 250 mg, and co-administering the mAb, either proactively or passively, according to a dosing regimen that achieves a therapeutically effective amount repeated three times a week, twice or once, once every two weeks, once every three weeks, or at least once a month.

A bispecific antibody targeting EGFR and c-Met. By means of modifying the amino acid sequence of an Fc segment of a binding arm, the heterodimeric interaction between an EGFR binding arm and a c-Met binding arm of the bispecific antibody is stronger than the interaction of the respective homodimers, such that a heterodimer can be assembled in vitro. The bispecific antibody is more effective in inhibiting the proliferation of EGFR and c-Met double positive tumor cells than a combination of an EGFR monoclonal antibody and a c-Met monoclonal antibody. The bispecific antibody mediates antibody-dependent cytotoxicity (ADCC), promotes target protein internalization, and inhibits the cell proliferation of the strain with acquired resistance to osimertinib. The prepared bispecific antibody is simple to prepare and stable in structure, a pure bispecific antibody is obtained by means of in-vitro assembly, and the bispecific antibody is expected to better meet clinical treatment needs, and therefore the bispecific antibody has good market prospects.

A method of treating patients suffering from cancers driven by deregulated Human Epidermal Growth Factor Receptor (HER1 / Human EGFR) comprising administering to a patient in need of such treatment a flexible and active regimen for combining a tyrosine kinase inhibitor (TKI) and anti-EGF antibodies for inhibition of the pathway activated by EGF-EGFR binding (mAb). The anti-EGF antibodies can be produced by active immunization or provided passively by the administration of antibodies that are anti-EGF. The method comprises TKI administered according to a continuous regimen based on an average daily dose in the range of 10 to 150 mg and the mAb is co-administered either actively or passively according to a dosing regimen achieving a therapeutic effective amount repeated thrice, twice or once a week, once in two weeks, once in three weeks or at least once monthly.

The invention provides an anti-tumor composition and application thereof, and belongs to the technical field of biological medicine. The invention provides an anti-tumor composition. The anti-tumor composition comprises a first component and a second component, the first component is prepared from 2-hydroxycinnamic acid; the second component comprises ferulic acid and / or cinnamic acid; the molar ratio of the first component to the second component is (1-2): (1-3). In the composition disclosed by the invention, the 2-hydroxycinnamic acid and the cinnamic acid can target EGFR (Epidermal Growth Factor Receptor), and at an EGFR binding site, the 2-hydroxycinnamic acid and the cinnamic acid enhance the binding stability through hydrophobic interaction; 2-hydroxycinnamic acid and ferulic acid can target PCNA, and at a PCNA binding site, 2-hydroxycinnamic acid and ferulic acid achieve a synergistic effect through pi-pi stacking interaction. The anti-tumor composition provided by the invention can be used for targeted therapy of tumors with EGFRY845 phosphorylation and / or PCNA high expression characteristics.

A bispecific antibody, a drug conjugate thereof, and uses thereof are provided. The bispecific antibody comprises an EGFR binding domain and a HER3 binding domain. The bispecific antibody and the drug conjugate thereof provided by the invention have good endocytosis effect, proliferation inhibition activity, tumor growth inhibition activity and good in-vivo safety.