dicycloplatin dicycloplatin dicycloplatin is a chemotherapy medication used to treat a number of cancers which includes the non-small-cell lung carcinoma and prostate cancer. dicycloplatinchemical structure of dicycloplatinclinical datatrade namesdicycloplatinother namesplatinum(2+) 1-carboxycyclobutanecarboxylate ammoniate (1:2:2), 1,1-cyclobutanedicarboxylic acid, compd. with (sp-4-2)-diammine(1,1-cyclobutanedi(carboxylato-kappao)(2-))platinum (1:1)routes ofadministrationintravenouspharmacokinetic databioavailability100% (iv)protein binding< 88.7%elimination half-life24.49 - 108.93 hoursexcretionrenalidentifiers iupac name azane;cyclobutane-1,1-dicarboxylate;cyclobutane-1,1-dicarboxylic acid;platinum(2+) cas number287402-09-9 ychemspider8476840 nunii0kc57i4unbchemical and physical dataformulac12h20n2o8ptmolar mass515.382 g·mol−13d model (jsmol)interactive imagecoordination form: interactive image smiles c1cc(c1)(c(=o)o)c(=o)o.c1cc(c1)(c(=o))c(=o).n.n.coordination form: c0ccc0c41oo(o2)c0(ccc0)(o3)oo4o23o1 inchi inchi=inchi=1s/2c6h8o4.2h3n.pt/c2*7-4(8)6(5(9)10)2-1-3-6;;;/h2*1-3h2,(h,7,8)(h,9,10);2*1h3;/q;;;;+2/p-2 ykey:iijqickywpgjdt-uhfffaoysa-l y some side effects which are observed from the treatment by dicycloplatin are nausea, vomiting, thrombocytopenia, neutropenia, anemia, fatigue, loss of appetite, liver enzyme elevation and alopecia. the drug is a platinum-based antineoplastic, and it works by causing mitochondrial dysfunction which leads to cell death. dicycloplatin was developed in china and it was used for phase i human trial clinical in 2006. the drug was approved for chemotherapy by the chinese fda in 2012. medical uses dicycloplatin can inhibit the proliferation of tumor cells via the induction of apoptosis. it is used to treat a number types of cancer which are non-small-cell lung carcinoma and prostate cancer. side effects similar to cisplatin and carboplatin, dicycloplatin also contains some side effects, which are nausea, vomiting, thrombocytopenia, neutropenia, anemia, fatigue, loss of appetite, liver enzyme elevation, and alopecia. however, with doses up to 350 mg/m(2), there is no significant toxicity; these effects are observed only at higher doses. furthermore, the nephrotoxicity of dicycloplatin is reported to be less than that of cisplatin, and its myelosuppressive potency is similar to that of carboplatin. chemical structure dicycloplatin consists of carboplatin and cyclobutane-1,1-dicarboxylic acid (cbdc) linked by the hydrogen bond. in the structure of dicycloplatin, there are two types of bond: o-h...o is the bond between the hydroxyl group of cbdc with carboxyl oxygen atom. it creates the one-dimensional polymer chain of carboplatin and cbdc. the second one is n-h...o which links between the ammonia group of carboplatin and oxygen of cbdc. it forms the two-dimensional polymer chain of carboplatin and cbdc. in aqueous solution, the 2d-hydrogen bonded polymeric structure of dicycloplatin is destroyed. firstly, the bond between ammonia group of carboplatin and oxygen of cbdc breaks, thus inducing the formation of one-dimensional dicycloplatin. after that, the strong hydrogen bond breaks and creates an intermediate state of dicycloplatin. finally, the rearrangement of different orientation of carboplatin and cbdc leads to the formation of intramolecular hydrogen bond and a supramolecule of dicycloplatin with two o-h...o and n-h...o is created. mechanism of action similar to carboplatin, dicycloplatin inhibits the proliferation of cancer cells by inducing cell apoptosis. when treated with dicycloplatin, some changes in the properties of hep g2 cells are observed: the declination of mitochondria membrane potential, the release of cytochrome c from mitochondria to cytosol, the activation of caspase-9, caspase-3 and the decrease of bcl-2. those phenomena indicate the role of mitochondrial in the apoptosis by intrinsic way. furthermore, the increase in caspase-8 activation is also observed. this can stimulate the apoptosis by activating downstream caspase-3 or by cleaving bid. as a result, the cleavage of bid (tbid) transfers to the mitochondria and induce mitochondrial dysfunction which promotes the release of cytochrome c from mitochondria to cytosol. from the dicycloplatin-treated hep g2 cell, an excessive amount of reactive oxygen species was detected, which plays an important role in the release of cytochrome c. in the mitochondria, the release of hemoprotein happens through 2-step process: firstly, the dissociation of cytochrome c from its binding to cardiolipin happens. due to the reactive oxygen species, the cardiolipin is oxidized, thus reducing the cytochrome c binding and increase the concentration of free cytochrome c notes zhao d, zhang y, xu c, dong c, lin h, zhang l, et al. 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"mitochondria, oxidative stress and cell death". apoptosis. 12 (5): 913–22. doi:10.1007/s10495-007-0756-2. pmid 17453160. intracellular chemotherapeutic agents / antineoplastic agents (l01)sps/mis(m phase)block microtubule assembly vinca alkaloids (vinblastine# vincristine# vindesine vinflunine§ vinorelbine#) block microtubule disassembly taxanes (cabazitaxel docetaxel# larotaxel ortataxel† paclitaxel# tesetaxel) epothilones (ixabepilone) dna replicationinhibitordna precursors/antimetabolites(s phase)folic acid dihydrofolate reductase inhibitor (aminopterin methotrexate# pemetrexed pralatrexate) thymidylate synthase inhibitor (pemetrexed raltitrexed) purine adenosine deaminase inhibitor (pentostatin) halogenated/ribonucleotide reductase inhibitors (cladribine clofarabine fludarabine) nelarabine thiopurine (mercaptopurine# tioguanine#) pyrimidine thymidylate synthase inhibitor (capecitabine# carmofur doxifluridine floxuridine fluorouracil# tegafur (+gimeracil/oteracil)) dna polymerase inhibitor (cytarabine# +daunorubicin) ribonucleotide reductase inhibitor (gemcitabine#) hypomethylating agent (azacitidine decitabine) deoxyribonucleotide ribonucleotide reductase inhibitor (hydroxycarbamide#) topoisomerase inhibitors(s phase)i camptotheca (belotecan camptothecin cositecan† etirinotecan pegol† exatecan gimatecan irinotecan# lurtotecan‡ rubitecan‡ silatecan§ topotecan) ii podophyllum (etoposide# teniposide) ii+intercalation anthracyclines (aclarubicin amrubicin† daunorubicin# (+cytarabine) doxorubicin# epirubicin idarubicin pirarubicin valrubicin zorubicin) anthracenediones (mitoxantrone losoxantrone pixantrone) amsacrine bisantrene crisnatol menogaril§ crosslinking of dna(ccns)alkylating nitrogen mustards: bendamustine# chlormethine cyclophosphamide# (ifosfamide# trofosfamide) chlorambucil# melphalan (melphalan flufenamide) prednimustine uramustine nitrosoureas: carmustine fotemustine lomustine (semustine) nimustine ranimustine streptozocin alkyl sulfonates: busulfan (mannosulfan treosulfan) aziridines: carboquone thiotepa triaziquone triethylenemelamine platinum-based carboplatin# cisplatin# dicycloplatin nedaplatin oxaliplatin# satraplatin nonclassical altretamine hydrazines (procarbazine#) etoglucid mitobronitol pipobroman triazenes (dacarbazine# mitozolomide§ temozolomide) intercalation streptomyces (dactinomycin# bleomycin# mitomycins plicamycin) photosensitizers/pdt aminolevulinic acid efaproxiral methyl aminolevulinate padeliporfin porphyrin derivatives (porfimer sodium talaporfin temoporfin verteporfin) otherenzyme inhibitors fi (tipifarnib§) cdk inhibitors (abemaciclib alvocidib† palbociclib ribociclib seliciclib†) pri bortezomib carfilzomib oprozomib ixazomib phi (anagrelide) impdi (tiazofurin§) li (masoprocol) parp inhibitor (niraparib +abiraterone acetate olaparib rucaparib) hdac (belinostat entinostat panobinostat romidepsin vorinostat) piki (pi3k) (alpelisib copanlisib duvelisib idelalisib umbralisib‡) receptor antagonists era (atrasentan) retinoid x receptor (bexarotene) sex steroid (testolactone) other/ungrouped adagrasib aflibercept arsenic trioxide asparagine depleters (asparaginase#/pegaspargase) axicabtagene ciloleucel belzutifan bexarotene brexucabtagene autoleucel celecoxib ciltacabtagene autoleucel demecolcine denileukin diftitox elesclomol§ elsamitrucin enasidenib epacadostat eribulin estramustine phosphate glasdegib idecabtagene vicleucel ivosidenib lonidamine lucanthone lurbinectedin mitoguazone mitotane oblimersen† omacetaxine mepesuccinate plitidepsin retinoids (alitretinoin selinexor sitimagene ceradenovec sotorasib tagraxofusp talimogene laherparepvec tazemetostat tiazofurine tigilanol tiglate tisagenlecleucel trabectedin tretinoin#) veliparib venetoclax verdinexor vosaroxin #who-em ‡withdrawn from market clinical trials: †phase iii §never to phase iii platinum compoundspt(0) pt(p(c6h5)3)4 pt(ii) pt(nh3)2(co2)2c4h6 cis-pt(nh3)2cl2 trans-pt(nh3)2cl2 k2pt(cn)4 pt(nh3)4ptcl4 pt(nh3)2co2ch2o c6h10(nh2)2ptc2o4 nh3ptcl2nc5h4ch3 pt(c2h3o2)2 ptbr2 ptcl2 ptf2 pti2 k2ptcl4 (ptcl(nh3)2c6h12(nh2)2)pt(nh3)2(no3)4 pt(oh)2 ptsm ptsorganoplatinum(ii) compounds ptcl2c8h12 kptcl3c2h4 pt(iv) pto2 (nh4)2ptcl6 h2ptcl6 ptbr4 ptcl4 ptf4 k2ptcl6 pt(c2h3o2)2cl2nh3nh2c6h11 na2ptcl6 pt(oh)4 pts2 ptse2 pt(v) ptf5 o2ptf6 xeptf6 pt(vi) ptf6 this article is issued from wikipedia. the text is licensed under creative commons - attribution - sharealike. additional terms may apply for the media files.