31246-66-9

Upstream product

• 26035-31-4 cisplatine 
• 7732-18-5 water 
• 7722-84-1 dihydrogen peroxide 
• 26035-31-4 transplatin 
• 7722-64-7 potassium permanganate 
• 15663-27-1 cisplatin 

Downstream Products

• 15663-27-1 cisplatin 
• 16893-05-3 cis-diaammineplatinum(IV) tetrachloride 

Relevant academic research and scientific papers

Tetravalent platinum complex containing BET inhibitor and application

The invention discloses a tetravalent platinum complex containing a BET inhibitor. The structure of the tetravalent platinum complex is as shown in a general formula I, wherein substituent groups are defined in the specification. The advantages of the tetravalent platinum complex are utilized, and the synergistic anti-tumor effect of the BET inhibitor and cis-platinum is exerted. The tetravalent platinum complex containing the BET inhibitor shows broad-spectrum and excellent in-vitro anti-tumor activity, the activity of the tetravalent platinum complex is obviously superior to that of cis-platinum, the BET inhibitor and the mixture of the cis-platinum and the BET inhibitor according to the ratio of 1: 1, and the tetravalent platinum complex has huge potential of being developed into a novel broad-spectrum anti-tumor drug.

Quadrivalent platinum prodrug bendazac platinum, preparation thereof, and preparation methods and applications of prodrug and preparation

The invention belongs to the technical field of medicines, and particularly relates to a tetravalent platinum prodrug bendazac platinum, a preparation thereof, and preparation methods and applications of the prodrug and the preparation. The structural formula of the prodrug is shown in the specification. The preparation method of the prodrug comprises the following steps: (1) synthesizing hydroxyl platinum; (2) synthesizing bendazac platinum; and (3) purifying the bendazac platinum. The preparation method of the nano preparation comprises the following steps: (1) preparing a bendazac platinum solution; and (2) preparing the nano preparation by taking bovine serum albumin as a carrier. The tetravalent platinum prodrug bendazac platinum and the nano preparation thereof provided by the invention are good in water solubility, small in toxic and side effects and high in anti-tumor efficacy, can be passively targeted to a tumor site, can increase the drug uptake ability of tumor cells, and show a good anti-tumor effect, and the inhibition rates of the tetravalent platinum prodrug bendazac platinum to various tumors can be higher than 90%.

Human serum albumin loaded tetravalent platinum nanoparticles and preparation method thereof

The invention relates to human serum albumin loaded tetravalent platinum nanoparticles and a preparation method thereof, the nanoparticles are formed by self-assembly of albumin and a tetravalent platinum drug modified with double aliphatic chains, the structural formula of the tetravalent platinum drug is as shown in formula I or formula II, and n and m are respectively and independently selected from integers of 1-15. The nanoparticles can respond to the environment in tumor cells to release platinum drugs, therefore effectively reduce the system toxicity, overcome the drug resistance of the tumor cells, and have the advantage of enhancing the killing effect on the tumor cells.

Low-toxicity Pt complex and preparation method and application thereof

The invention discloses a low-toxicity Pt complex, and belongs to the technical field of anticancer chemical drugs. The structure of the complex is as shown in a general formula (1) or a general formula (2), pterostilbene is introduced into the platinum (IV) complex, and the anti-tumor effect of the platinum complex is improved and the toxic and side effects of the platinum complex on normal cells are reduced by utilizing the anti-inflammatory and anti-oxidation double functions of the pterostilbene.

Tetravalent platinum complex containing artesunate as well as preparation method and application of tetravalent platinum complex

The invention discloses a tetravalent platinum complex containing artesunate. The structure of the tetravalent platinum complex is shown as a general formula I or II, wherein R is shown in the specification, and R1 is a branched chain or straight chain saturated C1-C20 alkyl group, or a branched chain or straight chain unsaturated C1-C20 alkyl group. The tetravalent platinum complex containing artesunate provided by the invention has an obvious proliferation inhibition effect on liver cancer HepG2, lung cancer A549, intestinal cancer HCT116, breast cancer MDA-MB-231 and cis-platinum drug-resistant lung cancer, the anti-tumor activity of part of compounds is obviously superior to that of cis-platinum, and the tetravalent platinum complex containing artesunate can be used as anti-tumor candidate drugs for deeper research.

Immunogenicity and cytotoxicity of a platinum(iv) complex derived from capsaicin

Platinum-based anticancer drugs constitute the cornerstone of chemotherapy for various cancers. Although cytotoxic agents are considered to have immunosuppressive effects, increasing evidence suggests that some cytotoxic compounds can effectively stimulate the antitumor immune response by inducing a special type of apoptosis called immunogenic cell death (ICD). A platinum(iv) complex (DCP) modified with the derivative of synthetic capsaicin (nonivamide) was designed to elicit ICD. The complex exhibited high cytotoxicity against a panel of human cancer cell lines including pancreas (PANC-1), breast (MCF-7), and liver (HepG2) cancer cells, and osteosarcoma (MG-63) cells. In addition to causing DNA damage, DCP also triggered the translocation of calreticulin (CRT) as well as the release of ATP and HMGB1 protein in PANC-1 cells, thus manifesting an efficient ICD-inducing effect on cancer cells. Furthermore, the DCP-treated PANC-1 cell-conditioned culture medium promoted the release of IFN-γ and TNF-α to induce the immune response of human peripheral blood mononuclear cells, thereby increasing their cytotoxicity to cancer cells. Concurrently, the phagocytosis of PANC-1 cells by macrophages was also augmented by DCP. The results demonstrate that DCP is an effective inducer of ICD and a potential agent for chemoimmunotherapy of cancers.

The invention discloses an amphipathic conjugate anti-tumor nano drug and a preparation method thereof. Nano-assembly and application

The anti-tumor prodrug comprises at least one of a cisplatin precursor, a carboplatin precursor and an oxaliplatin precursor. The amphipathic conjugate anti-tumor nano-drug is simple in chemical structure, can be assembled into a uniform nano structure in water, can greatly reduce the damage to normal cells by reducing cytotoxicity of an antitumor drug outside the tumor cells, and has EPR effect in vivo so as to promote blood circulation time in a human body. Compared with a small molecule anti-tumor drug, the conjugate can prolong the blood circulation time in the human body and has a passive targeting function, so that the enrichment of the conjugate in the tumor site is greatly improved.

PLATINUM PRODRUG PERFLUOROARYL PEPTIDE CONJUGATES

The disclosure provides platinum(IV) prodrug perfluoroaryl peptide conjugates that can be used to treat cell proliferative disorders, such as those associated with malignant tumor cells. The conjugates can improve the delivery of platinum(IV) prodrugs to glioma cells.

Let-7i miRNA and platinum loaded nano-graphene oxide platform for detection/reversion of drug resistance and synergetic chemical-photothermal inhibition of cancer cell

The drug resistance of chemotherapy is a major challenge to overcome for antineoplastic agents and the reverse of drug resistant is essential for cancer therapy. Herein, we developed a drug delivery system which can simultaneously detect/reverse the drug resistance and perform synergetic treatment of cancer. In this work, we integrated cyanine5 (Cy5) modified miRNA (let-7i) (Cy5-miRNA) and platinum onto nano-graphene oxide (NGO) (30-50 nm) platform to achieve simultaneously detection/reversion of drug resistance and synergetic treatment of cisplatin resistant SKOV3 cells (SKOV3DDP cells). The Cy5-miRNA adsorbed on NGO could selectively bind the drug resistance related mRNA follow by suppress the expression of drug resistance mRNA, and the binding simultaneously induced the release of Cy5-miRNA from the NGO, thus the fluorescence signal of Cy5 recovered and could be used for drug resistance monitoring. Moreover, the miRNA suppressed the Cyclin D1 protein expressions thus reversed the drug resistance. The loaded platinum(IV) (Pt(IV)) was converted to the therapeutic platinum(II) (Pt(II)) in both tumor acidic and reductive environment responsive behavior. NGO furtherly performed photothermal therapy under near infrared (NIR) laser irradiation and enhanced the therapeutic effect. All in all, this nanoplatform realized detection/reversion of the drug resistance as well as synergetic chemical-photothermal treatment of ovarian cancer cells, which holds great promise in the treatment of drug resistant cancer cells.

Targeting ROS-AMPK pathway by multiaction Platinum(IV) prodrugs containing hypolipidemic drug bezafibrate

Alterations in lipid metabolism, commonly disregarded in the past, have been accepted as a hallmark for cancer. Exploring cancer therapeutics that interrupt the lipid metabolic pathways by monotherapy or combination with conventional chemotherapy or immunotherapy is of great importance. Here we modified cisplatin with an FDA-approved hypolipidemic drug, bezafibrate (BEZ), via the well-established Pt(IV) strategy, affording two multi-functional Pt(IV) anticancer agents cis,cis,trans-[Pt(NH3)2Cl2(BEZ)(OH)] (CB) and cis,cis,trans-[Pt(NH3)2Cl2(BEZ)2] (CP) (BEZ = bezafibrate). The Pt(IV) prodrug CB exhibited an enhanced anticancer activity up to 187-fold greater than the clinical anticancer drug cisplatin. Both CB and CP had less toxicity to normal cells, showing higher efficacies and superior therapeutic indexes than cisplatin. Mechanism studies revealed that the bezafibrate-conjugated Pt(IV) complex CB, as a representative, could massively accumulate in A549 cells and genomic DNA, induce DNA damage, elevate intracellular ROS levels, perturb mitochondrial transmembrane potentials, activate the cellular metabolic sensor AMPK, and result in profound proliferation inhibition and apoptosis. Further cellular data also provided evidence that phosphorylation of AMPK, as a metabolic sensor, could suppress the downstream HMGB1, NF-κB, and VEGFA, which may contribute to the inhibition of angiogenesis and metastasis. Our study suggests that the antitumor action of CB and CP mechanistically distinct from the conventional platinum drugs and that functionalizing platinum-based agents with lipid-modulating agents may represent a novel practical strategy for cancer treatment.