38 results about "Receptor type" patented technology

The MYC and NMYC transcription factors (TFs) play a key role in cell proliferation and are overexpressed in most cancer cells. However, in normal cells their overexpression triggers safeguard mechanisms promoting cell death and cellular senescence, which are bypassed in cancer cells. Here, the inventors reveal that in normal cells MYC binds to the Inositol 1,4,5-Trisphosphate Receptor type 1 (ITPR1) gene and upregulates its expression, triggering an ER-mitochondria calcium (Ca2+) transfer, which is involved in MYC-induced cell death and senescence. Supporting a tumor suppressive role of MYC / ITPR1 axis, ITPR1 expression is generally decreased in cancer and reactivation of this pathway induces cancer cell death. Nevertheless, some cancer cells, generally expressing high levels of MYCN and / or MYC, also express high level of ITPR1, which correlates with high expression of BCL2, encoding an inhibitor of ITPR1. Strikingly, in high-risk MYCN-amplified neuroblastoma, ITPR1 expression is controlled by NMYC and its level correlates with worse patient survival. In these cells, blocking the interaction between BCL2 and ITPR1, via an BCL2-BH4 domain inhibitor induces mitochondrial Ca2+ accumulation and cell death, and decreases tumor size. Thus, the present invention relates to a method for treating MYChigh cancer, and in particular NMYC--amplified neuroblastoma in a subject by administering an BCL2-BH4 domain inhibitor.

The present invention relates to compounds and methods useful for dual inhibition of C-X-C receptor type 4 (CXCR4) and Bruton's tyrosine kinase (BTK). The invention also provides pharmaceutically acceptable compositions comprising compounds of the present invention and methods of using said compositions in the treatment of various disorders.

Compositions and methods for editing, e.g., altering, DNA sequences within TGFβR2 are provided. Compositions and methods for reducing or eliminating TGFβR2 protein expression in a cell are provided. Compositions and methods for immunotherapy are provided.

The present invention relates to antisense oligonucleotides (ASO) for use in treating, preventing, or ameliorating the progression of conditions such as type 2 diabetes mellitus (T2DM) and insulin resistance, leptin resistance, and obesity, Rater Syndrome, and cancer. Specifically, a thiomorpholino-containing ASO targets a protein tyrosine phosphatase non-receptor type 1 (PTPN1) gene transcript and induces exon skipping (including exon 2) of the transcript during RNA processing, thereby inhibiting expression of the protein tyrosine phosphatase-1B (PTP1B) protein.

Provided in the present invention are an siRNA for inhibiting the expression of the activin A receptor type 1C (ACVR1C) gene, and a conjugate thereof. The siRNA comprises a sense strand and an antisense strand. The antisense strand comprises at least 17 consecutive nucleotides that differ from nucleotide sequences set forth in SEQ ID NO: 1236-SEQ ID NO: 2470 by no more than 4 nucleotides. The antisense strand is 17-30 nucleotides in length; and the sense strand is 17-30 nucleotides in length, and is at least partially or completely complementary to the antisense strand. The siRNA, siRNA conjugate and pharmaceutical composition provided in the present invention exhibit good stability, great ACVR1C gene inhibitory activity, and satisfactory cytotoxicity and immunostimulatory activity.

Described herein, inter alia, are compounds for treating cancer and methods of use. This disclosure features chemical entities (e.g., small hairpin RNAs (shRNAs), micro RNA (miRNAs), small interfering RNA (siRNAs), small molecule inhibitors, antisense nucleic acids, peptides, viruses, CRISPR-sgRNAs, or combinations thereof) that inhibit one or more of m6A writers (e.g., methyltransferase like 3 (Mettl3 or MT-A70) or methyltransferase like-14 (Mettl14)), m6Am writers (e.g., phosphorylated CTD interacting factor I (PCIF 1), or Mettl3 / 14), m6A erasers (e.g., fat-mass and obesity-associated protein (FTO) or ALKB homolog 5 (ALKBH5)), m6Am erasers (e.g., FTO), m6A readers (e.g., YTH domain-containing family proteins (YTHs)), YTF domain family member 1 (YTHDF 1), YTF domain family member 2 (YTHDF 2), YTF domain family member 3 (YTHDF 3), or tyrosine-protein phosphatase non-receptor type 2 (PTPN2).

The present disclosure provides methods and compositions for reducing the addictive liability of opioid analgesics in a subject, for example, by co-administering to the subject the opioid and a serotonin receptor type 2 (5HT2) agonist or a serotonin (5HT) releasing agent. The disclosed methods include methods for preventing opioid abuse, methods for reducing the rewarding effect of an opioid, methods for reducing the addictive liability of an opioid, methods for eliminating or substantially reducing the tendency for a subject to develop physical dependence, tolerance, and / or withdrawal symptoms with respect to an opioid, and methods for eliminating or substantially reducing the tendency for a subject to use opioids in ways not prescribed, take opioids more often or in larger amounts than prescribed, and / or use opioids recreationally. The methods can be performed on a subject, such as a patient (e.g., a human patient).

Provided herein are useful for degrading protein tyrosine phosphatase, such as protein tyrosine phosphatase non-receptor type 2 (PTPN2) and / or protein tyrosine phosphatase non-receptor type 1 (PTPN1), and useful for treating related diseases, disorders and conditions that contribute to the treatment of PTPN1 or PTPN2 degrading agents, degradation agent compounds, compositions, and methods for treating cancer, such as cancer or metabolic diseases.

Provided herein are methods of using a combination comprising protein tyrosine phosphatase non-receptor type 2 (PTPN2) and / or protein tyrosine phosphatase non-receptor type 1 (PTPN1) and an additional therapeutic agent to treat a disease (e.g., cancer or metabolic disease) that produces an advantageous response to PTPN1 or PTPN2 inhibitor treatment.

This document relates to methods and materials involved in treating cancer. For example, methods and materials for using chimeric antigen receptor (CAR) T cells having reduced levels of an interleukin (IL) 4 polypeptide, having reduced levels of a transcription factor 7 (TCF7) polypeptide, having reduced levels of a protein tyrosine phosphatase non-receptor type 2 (PTPN2) polypeptide, and / or having reduced levels of a protein tyrosine phosphatase non-receptor type 3 (PTPN3) polypeptide are provided. Methods and materials for using such CAR T cells in an adoptive cell therapy (e.g., a CAR T cell therapy) to treat a mammal (e.g., a human) having cancer also are provided

The invention discloses a donor-receptor type carbon nitride photocatalyst as well as a preparation method and application thereof, and the preparation method of the donor-receptor type carbon nitride photocatalyst comprises the following steps: S1, preparing an amino-containing carbon nitride nanosheet; s2, the carbon nitride nanosheet and an aggregation-induced emission unit are subjected to a Schiff base reaction in a solvent, and the donor-acceptor type carbon nitride photocatalyst is obtained, the aggregation-induced emission unit in the step S2 is one or more of a triphenylamine derivative and a tetraphenyl ethylene derivative. The organic molecules with aggregation-induced emission characteristics are covalently modified, the conjugated structure of the organic molecules is adjusted, and the electron donating capability is regulated, so that the light absorption capability and the intramolecular charge transfer capability of the donor-acceptor type carbon nitride photocatalyst can be effectively improved, and the photocatalytic hydrogen production performance is remarkably improved.

The present application relates generally to the field of bone morphogenetic protein (BMP) antagonists (soluble ALK6 fusion proteins), compositions thereof, and methods for treating degenerative and / or demyelinating diseases of the nervous system.

To provide compounds, compositions and methods useful for inhibiting protein tyrosine phosphatase, e.g., protein tyrosine phosphatase non-receptor type 2 (PTPN2) and / or protein tyrosine phosphatase non-receptor type 1 (PTPN1), and for treating related diseases, disorders and conditions favorably responsive to PTPN1 or PTPN2 inhibitor treatment, e.g., a cancer or a metabolic disease.SOLUTION: The invention provides a compound represented by formula (1) or a pharmaceutically acceptable salt, solvate, hydrate, tautomer, ester, N-oxide, stereoisomer or isotopically enriched variant thereof.SELECTED DRAWING: None

The present invention relates to modified recombinant human MIS protein which has improved cleavage and increased bioactivity and increased potency as compared to wild-type human MIS protein. Other aspects of the invention relate to methods to prevent and treat cancers, such as cancers that express the MIS receptor type II (MISRII) by administering to a subject a composition comprising a recombinant human MIS protein. Another aspect of the present invention relates to methods to lower plasma androgen levels in a subject, and / or for the treatment of a subject with a disease characterized by excess androgen. Another aspect provides pharmaceutical compositions and kits and methods for use comprising a recombinant human MIS protein. Another aspect of the present invention relates to methods to decrease the dose of a chemotherapeutic agent by administering the chemotherapeutic agent with the recombinant MIS protein that lowers the effective dose of the chemotherapeutic agent.

The present disclosure relates to CRISPR related systems and components for targeting, editing and / or modulating PTPN2 (protein tyrosine phosphatase non-receptor type 2) gene expression. The disclosure also relates to methods and uses thereof related to engineered cells comprising T cells or T cell precursors.

The present invention relates to modified recombinant human MIS protein which has improved cleavage and increased bioactivity and increased potency as compared to wild-type human MIS protein. Other aspects of the invention relate to methods to prevent and treat cancers, such as cancers that express the MIS receptor type II (MISRII) by administering to a subject a composition comprising a recombinant human MIS protein. Another aspect of the present invention relates to methods to lower plasma androgen levels in a subject, and / or for the treatment of a subject with a disease characterized by excess androgen. Another aspect provides pharmaceutical compositions and kits and methods for use comprising a recombinant human MIS protein. Another aspect of the present invention relates to methods to decrease the dose of a chemotherapeutic agent by administering the chemotherapeutic agent with the recombinant MIS protein that lowers the effective dose of the chemotherapeutic agent.

The present invention addresses the problem of providing a method for simply and efficiently inducing oocytes and prespermatogonium cells to differentiate from primordial germ cell-like cells or primordial germ cells. This problem is solved by a method for producing oogonium cells or prespermatogonium cells, which comprises a step for culturing primordial germ cell-like cells or primordial germ cells in a culture medium containing a BMP receptor type 2 signaling agonist to obtain oogonium cells or prespermatogonium cells.

A population of genetically engineered T cells, comprising a disrupted protein tyrosine phosphatase non-receptor type 2 (PTPN2) gene and optionally a disrupted TRAC gene, a disrupted β2M gene, and / or a disrupted CD70 gene. Also provided herein are methods for making such genetically engineered T cells and therapeutic uses thereof.

The invention discloses an alkaline phosphatase response type near-infrared fluorescent probe and a preparation method and application thereof, the fluorescent probe is a compound XDM-P, the molecular structure of the fluorescent probe comprises a donor-pi-conjugate-receptor type near-infrared fluorophore constructed by taking xanthene and cyanoisophorone as parent nucleuses, and a recognition group linked by a phosphate bond; the preparation method comprises Knoevenagel condensation, phosphorylation and selective dealkylation reaction. The probe is subjected to specific hydrolysis under the action of alkaline phosphatase (ALP), the intramolecular charge transfer effect is recovered, and near-infrared fluorescence 'OFF-ON' response at 774 nm is realized. The probe provided by the invention has high sensitivity, good linear response and deep tissue penetrating ability, and can be used for intracellular ALP detection and non-invasive, real-time and semi-quantitative in-vivo fluorescence imaging of liver cancer tumor-bearing mouse and drug-induced liver injury mouse models.

The present invention relates to antisense oligonucleotides (ASOs) used to treat, prevent, or mitigate the progression of conditions such as type 2 diabetes mellitus (T2DM) and insulin resistance, leptin resistance and obesity, Rett syndrome, and cancer. Specifically, thiomorpholino-containing ASOs target the protein tyrosine phosphatase non-receptor type 1 (PTPN1) gene transcript during RNA processing and induce exon skipping (including exon 2), thereby inhibiting the expression of protein tyrosine phosphatase-1B (PTP1B) protein.

Provided is an anti-PD-L1 antibody which has excellent activity in blocking the interaction between PD-1 and PD-L1. A multifunctional molecule comprising the anti-PD-L1 antibody or fragment thereof fused to an extracellular structure of human TGF-beta receptor type 2 is also provided.

The present invention relates to new compounds of formula (1):as modulators of serotonin receptor 1B (5-HTR1B) also known as 5-hydroxytryptamine receptor 1B (5-HT1B). The compounds are of potential utility in the treatment of diseases and conditions mediated by serotonin receptor type 1B (5-HTR1B), such as cancer, including blood cancer and solid tumors, respiratory diseases and hepatic disorders.

The present disclosure relates to CRISPR-related systems and components for targeting, editing, and / or modulating expression of a PTPN2 (Protein Tyrosine Phosphatase Non-Receptor Type 2) gene. The present disclosure also relates to methods and applications thereof in connection with engineered immunocompetent cells including T cells or T cell precursors.

Provided are compounds, compositions, and methods useful for inhibiting protein-tyrosine phosphatases, e.g., non-receptor protein-tyrosine phosphatase type 2 (PTPN2) and / or non-receptor protein-tyrosine phosphatase type 1 (PTPN1), and for treating associated diseases, disorders, and conditions that respond favorably to treatment with PTPN1 or PTPN2 inhibitors, e.g., cancers or metabolic diseases.SOLUTION: A [1-fluoro-3-hydroxynaphthalen-2-yl] - 1 λ 6,2,5 - thiadiazolidine - 1,1,3 - trione derivative represented by the following formula: (R1 to R3 are each independently H, halogen, substitutable C1 to 6 alkyl, substitutable C1 to 6 alkoxy, or the like; R4 and R5 are each independently H, halogen, substitutable C1 to 6 alkyl, or the like; R6 and R7 are each independently H. ) SELECTED DRAWING: None

The present invention provides, among other things, a half-life extended anti- interleukin-1 receptor type-1 (IL1R1) antibody engineered with Fc mutations that render superior pharmacokinetic profiles without decreasing stability and manufacturability of the anti-IL1R1 antibody.

The invention relates to a novel epitope of PTPRZ1 which presents good immunogenicity and is useful for immunotherapy of cancer.

The present invention refers to a bispecific in tandem receptor CAR, named RfuCAR, which includes a scFv that recognizes and ligates surface molecules on tumoral cells (CD33, CD123 or another tumoral target) and the IL-1 receptor type 2 (IL-1R2). According to this, the IL1-R2 was chosen as the ideal receptor to compose the RfuCAR construction, being able to capture the IL-1β with high affinity and specificity. These proprieties indicate it as a good candidate to reduce the neurotoxicity and CRS effects of CAR-T therapies. Additionally, the present invention deals with a method for modulating the tumoral microenvironment, for example, in case of acute myeloid leukemia, or other cancer type like but not restricted to acute lymbloblastic leukemia, pancreatic, lung and ovarian cancer.