15 results about "Neurocatin" patented technology

Topical aprepitant formulations and methods of treating epidermal growth factor receptor inhibitor-associated skin toxicities. In some embodiments, the present disclosure pertains to a topical composition comprising a neurokinin-1 receptor antagonist selected from aprepitant or a pharmaceutically acceptable salt thereof or fosaprepitant or a pharmaceutically acceptable salt thereof, and at least one excipient, wherein the composition is a non-aqueous emulsion.

An improved method of administering a neurokinin-1 receptor antagonist, preferably defortupitant, by intravenous injection, preferably for a shortened period of time.

A pharmaceutical composition comprising a neurokinin-1 antagonist prodrug compound. A pharmaceutical composition comprising a compound of formula I and a stabilizer, and a preparation method therefor.

Provided herein are methods for treating drug addiction in a subject, the method comprising activating neurokinin B (NKB)-expressing neurons of the subject. Also provided herein are compositions useful for the treatment of drug addiction in a subject by activating neurokinin B (NKB)-expressing neurons.

The invention relates to an N-terminal palmitoylated / C-terminal ethylamine dual-modified LMN-NKA polypeptide derivative, a pharmaceutically acceptable salt thereof and a preparation method of the LMN-NKA polypeptide derivative. The chemical name of the LMN-NKA polypeptide derivative is N-palmitoyl-L-aspartic acid-L-lysine-L-phenylalanine-L-valine-glycine-N-methyl-L-leucine-L-n-leucine-ethylamine, and the structural formula of the LMN-NKA polypeptide derivative is Pal-Asp-Lys-Ph-Val-Gly-N-Me-Leu-Nle-NHCH2 CH3, and the structural formula of the LMN-NKA polypeptide derivative is shown in the description. According to the dual-modification strategy, the NK2 receptor binding capacity of the core active fragment of the neurokinin A can be specifically reserved, the enzymolysis stability, the fat solubility and the in-vivo metabolism stability are synergistically improved, the transmembrane efficiency is remarkably improved, and precise balance of water solubility and fat solubility is achieved. The polypeptide derivative and the salt thereof are especially suitable for preparing a long-acting therapeutic drug for NK2 receptor related chronic diseases.

The invention relates to an N-terminal lauroylation / C-terminal ethylamine dual-modified LMN-NKA polypeptide derivative, a pharmaceutically acceptable salt thereof and a preparation method of the LMN-NKA polypeptide derivative. The chemical name of the LMN-NKA polypeptide derivative is N-lauroyl-L-aspartic acid-L-lysine-L-phenylalanine-L-valine-glycine-N-methyl-L-leucine-L-n-leucine-ethylamine, and the structural formula of the LMN-NKA polypeptide derivative is Lau-Asp-Lys-Phe-Val-Gly-NMe-Leu-Nle-NHCH2 CH3, and the structural formula of the LMN-NKA polypeptide derivative is shown in the specification. According to the dual-modification strategy, the NK2 receptor binding capacity of the core active fragment of the neurokinin A can be specifically reserved, the enzymolysis stability, the fat solubility and the in-vivo metabolism stability are synergistically improved, the transmembrane efficiency is remarkably improved, and precise balance of water solubility and fat solubility is achieved. The polypeptide derivative and the salt thereof are especially suitable for preparing a long-acting therapeutic drug for NK2 receptor related chronic diseases.

Methods for decreasing or inhibiting herpesviridae infection, or associated condition, disease, or pathogenesis or other adverse effect of herpesviridae infection including reactivation of herpesviridae in a subject by administering to the subject a synergistic combination of Neurokinin-1 Receptor antagonist and a nucleoside analog.

Disclosed herein are methods of administering pharmaceutical formulations of a neurokinin-1 (NK-1) receptor antagonist to a subject in need of treatment of emesis.

This disclosure relates to compounds useful as modulators of neurokinin receptor 3 (NK3) for the treatment of disease or disorder.

The invention relates to an N-terminal lauroylation modified LMN-NKA polypeptide derivative, a pharmaceutically acceptable salt of the N-terminal lauroylation modified LMN-NKA polypeptide derivative and a preparation method of the N-terminal lauroylation modified LMN-NKA polypeptide derivative, and the name of the LMN-NKA polypeptide derivative is N-lauroyl-L-aspartic acid, L-lysine, L-phenylalanine, L-valine, glycine, N-methyl-L-leucine and L-n-leucine. The structural formula of the compound is Lau-Asp-Lys-Phe-Val-Gly-N-Me-Leu-Nle, and the structural formula of the compound is shown in the specification. Through a single precise modification strategy of N-terminal lauroylation (C12 medium-long-chain fatty acid chain), the NK2 receptor binding capacity of a core active fragment of the neurokinin A can be specifically reserved, the enzymolysis stability, the fat solubility and the in-vivo metabolism stability are synergistically improved, the transmembrane efficiency is improved, the balance of water solubility and fat solubility is realized, and the application prospect is wide. Furthermore, the polypeptide derivative and the salt thereof can be used for preparing a long-acting treatment medicine for NK2 receptor related chronic diseases.

The invention relates to an N-terminal palmitoylation modified LMN-NKA polypeptide derivative, a pharmaceutically acceptable salt of the N-terminal palmitoylation modified LMN-NKA polypeptide derivative and a preparation method of the N-terminal palmitoylation modified LMN-NKA polypeptide derivative, and the chemical name of the LMN-NKA polypeptide derivative is N-palmitoylation-L-aspartic acid-L-lysine-L-phenylalanine-L-valine-glycine-N-methyl-L-leucine-L-n-leucine. The structural formula of the compound is Pal-Asp-Lys-Phe-Val-Gly-N-Me-Leu-Nle, and the structural formula of the compound is shown in the specification. The NK2 receptor binding capacity of a core active fragment of neurokinin A (NKA) is specifically reserved through N-terminal single palmitoylation modification, meanwhile, the enzymolysis stability and fat solubility are remarkably improved, the transmembrane efficiency is improved compared with that of a natural LMN-NKA fragment, and the problem of water solubility caused by long-chain fatty acid modification is solved. The polypeptide derivative and the salt thereof are especially suitable for preparing a long-acting therapeutic drug for NK2 receptor related chronic diseases.

It relates to a novel method for personalizing a treatment for chemotherapy-induced nausea and vomiting (CINV) in a patient. SNP variations in genes HTR3A, HTR3B and TACR1 are utilized to predict the response to a particular anti-emetic regimen for a patient. Treatment regimens utilizing antagonists of 5-hydroxytryptamine type 3 (5-HT3R) receptor and neurokinin-1 (NK-1) receptor, with or without the addition of olanzapine are selected based on the patient genotype. In addition, a method has been generated to determine the genotypes of these genes and SNPs from VCF file output from high throughput sequencing.

The present disclosure relates to a crystal form of a neurokinin-1 antagonist prodrug compound. Specifically, the present disclosure relates to a novel crystal form of a compound represented by formula I and a preparation method. The novel crystal form of the present disclosure has a good physicochemical property and better facilitates clinical treatment.

The present disclosure relates to compounds useful as modulators of neurokinin receptor 3 (NK3) for the treatment of conditions or disorders.