8 results about "Lonidamine" patented technology

The invention discloses a nucleolin aptamer modified carboxymethyl chitosan-based glycolysis regulation nano-drug delivery system as well as a preparation method and application thereof, and relates to the field of tumor treatment. The nucleolin aptamer AS1411 is coupled with glycolysis regulation nano-particles through covalent bonds, and the carboxymethyl chitosan-based glycolysis regulation nano-drug delivery system comprises a carboxymethyl chitosan-based glycolysis regulation nano-drug delivery system, a carboxymethyl chitosan-based glycolysis regulation nano-drug delivery system and a carboxymethyl chitosan-based glycolysis regulation nano-drug delivery system, the glycolysis regulation nano-particles take carboxymethyl chitosan as a carrier skeleton, the carrier skeleton is loaded with a lonidamine derivative through grafting modification, and the nano drug delivery system can synchronously entrap paclitaxel. According to the invention, a synergistic treatment system integrating active targeting, metabolic regulation and chemotherapy is constructed, and by virtue of a multi-mechanism synergistic effect, an antitumor drug for inhibiting tumor cell activity, glycolysis or tumor metabolism reprogramming is prepared; the huge potentials of overcoming the drug resistance bottleneck of traditional chemotherapy, enhancing the curative effect and reducing the toxic and side effects are shown.

This invention discloses a ternary nanoparticle, its preparation method, and its applications, relating to the field of biomedical technology. The invention constructs a carrier-free, fully active ternary nanoparticle (diPCL NPs). This nanoplatform connects PTX dimer (diPTX), celecoxib (CXB) dimer (diCXB), and lonidamine (LND) dimer (diLND) via disulfide bonds for chemoimmunotherapy of drug-resistant tumors. diPCL NPs accumulate at tumor sites through enhanced permeability and retention (EPR) effects and circulate continuously in the bloodstream. In the high GSH tumor microenvironment, disulfide bond cleavage releases the active drug, exerting chemotherapeutic, immune-activating, sensitizing, and metabolic-regulating effects. diPCL NPs exhibit high antitumor efficacy and good safety profile within the therapeutic window in both breast cancer and paclitaxel-resistant models.

The application discloses a nano-focal anaphylaxis drug targeting CD47 protein and preparation and application thereof, and belongs to the technical field of drugs. The nano-focal anaphylaxis drug is a micellar nanoparticle formed by self-assembly of an amphiphilic carrier material and a focal anaphylaxis prodrug, the amphiphilic carrier material is composed of an amphiphilic polymer with a hydrophilic end modified with a CD47 targeting peptide and an amphiphilic polymer without modification, and the focal anaphylaxis prodrug is a prodrug formed by reduction response chemical bond connection of lonidamide or 3-bromopyruvic acid. The nano-focal anaphylaxis drug provided by the application can realize precise tumor treatment, the CD47 targeting peptide realizes efficient targeted delivery and accumulation of the drug in the tumor, the release of the focal anaphylaxis prodrug is triggered by higher reduction medium level in tumor tissues, and tumor cells are induced to undergo focal anaphylaxis. In normal tissues, the nano drug cannot induce normal cell focal anaphylaxis, and therefore the tumor selectivity of the nano drug is significantly enhanced.

The invention relates to a membrane fusion liposome delivery system and a preparation method and application thereof, and belongs to the technical field of liposome preparation. The invention provides a membrane fusion liposome delivery system. The system takes lipidosome as a carrier, the surface of the lipidosome is modified with cRGD targeting molecules, and the interior of the lipidosome is loaded with a TPP-modified antitumor drug lonidamine; a DNA device CLTD is anchored on a liposome membrane through cholesterol, and the device is formed by a short-chain CAP containing an APE1 restriction enzyme cutting site and a long-chain LTD containing a CD63 aptamer and a RelA aptamer through base complementary pairing. The APE1 enzyme highly expressed in a tumor microenvironment is used as a specific trigger signal, and precise activated release of the drug in tumor cells and space-time controllable degradation of RelA protein are achieved. According to the system, chemical drug inhibition and nucleic acid aptamer mediated protein degradation are synergistically linked, off-target toxicity is effectively overcome, and a new strategy is provided for precise treatment of cancers.

This invention belongs to the field of drug synthesis, specifically relating to a mitochondrial-targeted chlordamine and cinnamaldehyde conjugated prodrug, its preparation method, and its application. The structural formula of the chlordamine and cinnamaldehyde conjugated prodrug is as follows. This invention provides a mitochondrial-targeted chlordamine and cinnamaldehyde conjugated prodrug that, through triphenylphosphine targeting mitochondria, delivers cinnamaldehyde and chlordamine to tumor cells, causing mitochondrial dysfunction and inhibiting tumor cell growth. By introducing various substituents onto the aromatic ring, the spatial conformation of the molecule is improved, enhancing its activity. Chlordamine acts on mitochondria, affecting mitochondrial energy metabolism; through triphenylphosphine targeting tumor cells and synergistic action with cinnamaldehyde, it reduces the side effects of anticancer drugs.

This invention belongs to the field of pharmaceutical technology, and more specifically, relates to a chlordamine derivative targeting tumor mitochondria, its preparation method, and its application. The chlordamine derivative targeting tumor mitochondria provided by this invention has the structure shown in formula (I): wherein R is phenyl, or a phenyl substituted with one or more substituents selected from halogen, C1-C4 alkyl, nitro, and trifluoromethyl. This type of derivative induces oxidative stress in tumor stem cells by targeting mitochondria, disrupting mitochondrial morphology and function, and can induce apoptosis of tumor stem cells at extremely low concentrations. Compared with chlordamine, the mitochondrial-targeting chlordamine derivative has superior anti-tumor growth and metastasis capabilities and can significantly improve the survival time of tumor-bearing mice.

The invention discloses a mitochondrial targeted anti-cancer drug based on cyanine and lonidamine and a preparation method and application thereof, and belongs to the technical field of drugs for treating tumors. Cyanine molecules and 3-mercaptobenzoic acid are subjected to a nucleophilic substitution reaction to prepare a cyanine derivative; the preparation method comprises the following steps: carrying out a coupling reaction on a cyanine derivative and a selenocystamine compound to prepare a cyanine-connexon conjugate with an amino terminal; the cyanine-connexon conjugate and lonidamine are subjected to a coupling reaction, and the targeted anti-cancer drug is obtained. According to the mitochondrial targeting anti-cancer drug based on cyanine and lonidamine and the preparation method and application thereof, after the drug targets tumor cell mitochondria, cyanine molecules generate a photodynamic effect and a photothermal effect at the same time under the irradiation of near-infrared light, ROS and high temperature are generated in situ, the mitochondrial structure and function are directly damaged, and the drug can be used for preparing the mitochondrial targeting anti-cancer drug based on cyanine and lonidamine. The ROS also synchronously triggers diselenide bond breakage, lonidamine is accurately released, and mitochondrial dysfunction and metabolic crisis are further aggravated.

The invention relates to a nano preparation and a preparation method and application thereof, in particular to the technical field of biomedical materials. The nano preparation has a core-shell structure and comprises a core and a shell, the core comprises a photosensitizer and a glycometabolism inhibitor, the shell comprises an amphiphilic polymer, the photosensitizer is a near-infrared two-region fluorescent dye TTQ-BT-TPA, the glycometabolism inhibitor comprises lonidamine, the amphiphilic polymer comprises 1, 2, 4-trimethyl-1, 3-pentanediol monoisobutyrate, and the 1, 2, 4-trimethyl-1, 3-pentanediol monoisobutyrate is a near-infrared two-region fluorescent dye TTQ-BT-TPA. The composition is prepared from 1, 2-distearoyl-sn-glycerol-3-phosphoethanolamine-polyethylene glycol 2000 and 2-distearoyl-sn-glycerol-3 The invention provides a nano preparation. In the prior art, a traditional photodynamic therapy is limited in curative effect in a tumor anoxic zone due to dependence on oxygen, and tumor cells maintain a high-level anti-oxidation defense system due to metabolism reprogramming and are insensitive to ferroptosis; and the problem of poor synergistic effect caused by lack of accurate intervention on tumor metabolism and reduction of the yield of fluorescence and active oxygen in a photosensitizer aggregation state of an existing synergistic treatment system is solved.