シスプラチン
|
|
| IUPAC命名法による物質名 |
|
(SP-4-2)-Diamminedichloroplatinum
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| 臨床データ |
| 胎児危険度分類 |
|
| 法的規制 |
|
| 投与方法 |
点滴静注 |
| 薬物動態データ |
| 生物学的利用能 |
- |
| 血漿タンパク結合 |
98%（24時間） |
| 代謝 |
- |
| 半減期 |
20〜30分 |
| 排泄 |
尿中 |
| 識別 |
| CAS番号 |
15663-27-1 |
| ATCコード |
L01XA01 |
| PubChem |
CID: 84691 |
| DrugBank |
APRD00359 |
| KEGG |
D00275 |
| 化学的データ |
| 化学式 |
Cl2H6N2Pt |
| 分子量 |
300.05 |
シスプラチン（cisplatin : CDDP）は白金錯体に分類される抗悪性腫瘍剤（抗がん剤）。シスプラチンの「シス」は、立体化学の用語のシスに由来する。錯体の中心金属は白金、配位子はアンミンと塩化物イオンであり、物質名はシス-ジアミンジクロロ白金(II)（cis-diamminedichloro-platinum(II)、cis-[PtCl2(NH3)2]）である。なお、日光によって分解されるため、直射日光を避けて保存する必要があり、点滴にかかる時間を長く取る必要がある場合は点滴容器の遮光が必要となることもある。
商品名は、ブリプラチン（ブリストル・マイヤーズ）、ランダ（日本化薬）など。白金製剤としては、ほかにカルボプラチン、ネダプラチン、オキサリプラチンがある。 薬理作用を発現するのはシス型だけでトランス型は抗がん作用を示さない。
目次
- 1 開発経緯
- 2 合成経路
- 3 作用機序
- 4 効能・効果
- 5 主な副作用
- 5.1 腎毒性
- 5.2 悪心・嘔吐
- 5.3 聴器毒性
- 6 適用上の注意
- 7 関連事項
- 8 脚注
- 9 外部リンク
- 10 参考資料
開発経緯
シスプラチンは、1845年にイタリアの化学者ミケーレ・ペイローネ（Michele Peyrone、1813-1883年）により錯体の研究材料として合成され[1]、「ペイロン塩（Peyrone's salt）」と呼ばれた。
1965年、アメリカ合衆国のバーネット・ローゼンバーグ（w:Barnett Rosenberg）らは、細菌に対して電場が及ぼす影響を調べている時に、偶然プラチナ電極の分解産物が大腸菌の増殖を抑制し、フィラメントを形成させることを発見した。その後1969年には、ローゼンバーグらにより白金化合物の大腸菌に対する細胞分裂阻止作用を応用して癌細胞の分裂抑制に対する研究が行われ、その結果ペイロン塩、つまりシスプラチンが動物腫瘍において比較的広い抗腫瘍スペクトルを有する化合物であることが判明した。
1972年にはアメリカ国立癌研究所(NCI)の指導で臨床試験が開始されたが、強い腎毒性のため、いったんは開発が中断された。しかし、その後シスプラチン投与時に大量の水分負荷と、さらに利尿薬を使用することによって腎障害を軽減することが可能となった。その後の臨床開発により、1978年にカナダ、アメリカ等で承認され、1983年に日本で承認された。
合成経路
シスプラチンの合成反応は、トランス効果の典型例である。まず、テトラクロリド白金(II)酸カリウム（[PtCl4]2−）を出発物質とする。最初のNH3基は4つのCl基どれとも無作為に置換される。しかし、Cl−はNH3より大きなトランス効果を持ち、そのトランス位を置換活性とするため、NH3基の置換は、すでに存在しているNH3基に対してトランスの位置にはあまりおこらず、Cl基のトランスの位置におきやすい。したがって、2番目のNH3基はシス型に置換される。一方、[Pt(NH3)4]2+が出発物質であれば、Cl基のトランス効果のため2番目のCl基は最初のCl基のトランスの位置に入り、生成物はトランス型になる。
en:Image:trans_effect.png
作用機序
シスプラチンは、DNAの構成塩基であるグアニン、アデニンのN-7位に結合する。2つの塩素原子部位でDNAと結合するため、DNA鎖内には架橋が形成される。シス体に比べ、トランス体は架橋が形成されにくいため、投与量の制限により臨床的に用いることはできない。
効能・効果
- 睾丸腫瘍、膀胱癌、腎盂・尿管腫瘍、前立腺癌、卵巣癌、頭頸部癌、非小細胞肺癌、食道癌、子宮頸癌、神経芽細胞腫、胃癌、小細胞肺癌、骨肉腫、胚細胞腫瘍（精巣腫瘍、卵巣腫瘍、性腺外腫瘍）
- 悪性胸膜中皮腫･･ペメトレキセドと併用
- 以下の悪性腫瘍に対する他の抗悪性腫瘍剤との併用療法
- 悪性骨腫瘍、子宮体癌（術後補助化学療法、転移・再発時化学療法）･･･ドキソルビシンと併用
- 再発・難治性悪性リンパ腫、小児悪性固形腫瘍（横紋筋肉腫、神経芽腫、肝芽腫その他肝原発悪性腫瘍、髄芽腫等）
- M-VAC療法（シスプラチン、メトトレキサート、ビンブラスチン及びドキソルビシンとの併用療法）
禁忌：重篤な腎障害
主な副作用
腎毒性
- シスプラチンは主に近位尿細管細胞を障害する。
- 腎組織内でのシスプラチン濃度を低下させ、毒性を軽減することを目的に水分負荷（水分を与えておくこと、ハイドレーションとも言う）及び強制利尿を行う。このため投与時は尿量を調べることが必須となる。総投与量が 300〜700 mg/m2 までは腎機能障害の発現頻度は低いとされている。なお、フロセミドによる強制利尿を行う場合には腎障害、聴器障害が増強されることがあるので、輸液等による水分補給を十分に行うことが重要となる。
悪心・嘔吐
- 延髄外側網様体に位置する嘔吐中枢が刺激されて発現する。
- 急性の悪心・嘔吐に対しては、オンダンセトロン、グラニセトロン、アザセトロンといった5-HT3受容体拮抗薬を投与することにより、発現を大幅に減少させることができる。遅延性の嘔吐や予測性の嘔吐に対しては、メチルプレドニゾロンやデキサメタゾン等のステロイドホルモンと5-HT3受容体拮抗薬あるいはメトクロプラミド等との併用が臨床的によく用いられている。
聴器毒性
- 聴力低下、難聴、耳鳴り
- 蝸牛の外側有毛細胞の障害と考えられ、総投与量で300mg/m2 以上になると発現頻度が高くなる。
- 不可逆的であり、根本的な治療法は見つかっていない。障害が軽度な場合は投与中止で改善する可能性もあるので、定期的な聴力検査（オーディオグラム）を行い、障害の徴候があらわれたら、投与継続の是非を考慮する必要がある。
適用上の注意
調製時の注意
- 本剤を点滴静注する際、塩化物イオン濃度が低い輸液を用いるとSN2反応で加水分解し、細胞内に到達する前に、輸液中で塩化物イオンが水に置換した活性型となってしまい、腎毒性が現れやすくなるとともに、細胞内に入りにくくなってしまうため、必ず塩化物イオンがある程度含まれる輸液を用いること。また、この機序を利用した低張シスプラチン療法というものが考案された事もある[2]。
関連事項
脚注
- ^ Michele Peyrone (1813–1883), Discoverer of Cisplatin, "Platinum Metals Review", 2010, 54, (4) 250-256
- ^ Katano K. “Pharmacokinetics of hypotonic cisplatin chemotherapy administered into the peritoneal and the pleural cavities in experimental model.”. 2011年11月4日閲覧。
外部リンク
参考資料
- 『ブリプラチン®注』医薬品インタビューフォーム・新様式第2版（ブリストル・マイヤーズ）
|
この項目は、薬学に関連した書きかけの項目です。この項目を加筆・訂正などしてくださる協力者を求めています（プロジェクト:薬学／Portal:医学と医療）。 |
|
この項目は、医学に関連した書きかけの項目です。この項目を加筆・訂正などしてくださる協力者を求めています（プロジェクト:医学／Portal:医学と医療）。 |
Cisplatin
|
|
| Systematic (IUPAC) name |
|
(SP-4-2)-diamminedichloroplatinum(II)
|
| Clinical data |
| Trade names |
Platinol |
| AHFS/Drugs.com |
monograph |
| MedlinePlus |
a684036 |
Pregnancy
category |
|
| Legal status |
|
Routes of
administration |
Intravenous |
| Pharmacokinetic data |
| Bioavailability |
complete |
| Protein binding |
> 95% |
| Biological half-life |
30-100 hours |
| Excretion |
Renal |
| Identifiers |
| CAS Number |
15663-27-1 Y |
| ATC code |
L01XA01 |
| PubChem |
CID: 84691 |
| DrugBank |
DB00515 Y |
| ChemSpider |
76401 N |
| UNII |
Q20Q21Q62J Y |
| KEGG |
D00275 Y |
| ChEBI |
CHEBI:27899 Y |
| ChEMBL |
CHEMBL2068237 N |
| PDB ligand ID |
CPT (PDBe, RCSB PDB) |
| Chemical data |
| Formula |
H6Cl2N2Pt |
| Molecular mass |
300.01 g/mol |
SMILES
-
[NH3+][Pt-2]([NH3+])(Cl)Cl
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InChI
-
InChI=1S/2ClH.2H3N.Pt/h2*1H;2*1H3;/q;;;;+2/p-2 Y
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Key:LXZZYRPGZAFOLE-UHFFFAOYSA-L Y
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| N (what is this?) (verify) |
Cisplatin, cisplatinum, platamin, neoplatin, cismaplat[1] or cis-diamminedichloroplatinum(II)[2] (CDDP) is a chemotherapy drug. It was the first member of a class of platinum-containing anti-cancer drugs, which now also includes carboplatin and oxaliplatin.[3] These platinum complexes react in vivo, binding to and causing crosslinking of DNA, which ultimately triggers apoptosis (programmed cell death).
It is on the World Health Organization's List of Essential Medicines, a list of the most important medications needed in a basic health system.[4]
Contents
- 1 Medical use
- 2 Side effects
- 3 Mechanism of action
- 3.1 Cisplatin resistance
- 3.2 Transplatin
- 4 History
- 5 Synthesis
- 6 See also
- 7 References
- 8 External links
Medical use
Cisplatin is administered intravenously as short-term infusion in normal saline for treatment of solid malignancies. It is used to treat various types of cancers, including sarcomas, some carcinomas (e.g., small cell lung cancer, and ovarian cancer), lymphomas, bladder cancer, cervical cancer,[5] and germ cell tumors.
Cisplatin is particularly effective against testicular cancer; the cure rate was improved from 10% to 85%.[6]
In addition, cisplatin is used in Auger therapy.
Side effects
Cisplatin has a number of side-effects that can limit its use:
- Nephrotoxicity (kidney damage) is a major concern. The dose is reduced when the patient's creatinine clearance (a measure of renal function) is reduced. Adequate hydration and diuresis is used to prevent renal damage. The nephrotoxicity of platinum-class drugs seems to be related to reactive oxygen species and in animal models can be ameliorated by free radical scavenging agents (e.g., amifostine). Nephrotoxicity is a dose-limiting side effect.[7]
- Neurotoxicity (nerve damage) can be anticipated by performing nerve conduction studies before and after treatment. Common neurological side effects of cisplatin include visual perception and hearing disorder, which can occur soon after treatment begins.[8] While triggering apoptosis through interfering with DNA replication remains the primary mechanism of cisplatin, this has not been found to contribute to neurological side effects. Recent studies have shown that cisplatin noncompetitively inhibits an archetypal, membrane-bound mechanosensitive sodium-hydrogen ion transporter known as NHE-1.[8] It is primarily found on cells of the peripheral nervous system, which are aggregated in large numbers near the ocular and aural stimuli-receiving centers. This noncompetitive interaction has been linked to hydroelectrolytic imbalances and cytoskeleton alterations, both of which have been confirmed in vitro and in vivo. However, NHE-1 inhibition has been found to be both dose-dependent (half-inhibition = 30 µg/mL) and reversible.[8]
- Nausea and vomiting: cisplatin is one of the most emetogenic chemotherapy agents, but this symptom is managed with prophylactic antiemetics (ondansetron, granisetron, etc.) in combination with corticosteroids. Aprepitant combined with ondansetron and dexamethasone has been shown to be better for highly emetogenic chemotherapy than just ondansetron and dexamethasone.
- Ototoxicity (hearing loss): there is at present no effective treatment to prevent this side effect, which may be severe. Audiometric analysis may be necessary to assess the severity of ototoxicity. Other drugs (such as the aminoglycoside antibiotic class) may also cause ototoxicity, and the administration of this class of antibiotics in patients receiving cisplatin is generally avoided. The ototoxicity of both the aminoglycosides and cisplatin may be related to their ability to bind to melanin in the stria vascularis of the inner ear or the generation of reactive oxygen species.
- Electrolyte disturbance: Cisplatin can cause hypomagnesaemia, hypokalaemia and hypocalcaemia. The hypocalcaemia seems to occur in those with low serum magnesium secondary to cisplatin, so it is not primarily due to the cisplatin.
- Hemolytic anemia can be developed after several courses of cisplatin. It is suggested that an antibody reacting with a cisplatin-red-cell membrane is responsible for hemolysis.[9]
Mechanism of action
|
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This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (November 2014) |
Following administration, one of the chloride ligands is slowly displaced by water (an aqua ligand), in a process termed aquation[10] . The aqua ligand in the resulting [PtCl(H2O)(NH3)2]+ is itself easily displaced, allowing the platinum atom to bind to bases. Of the bases on DNA, guanine is preferred. Subsequent to formation of [PtCl(guanine-DNA)(NH3)2]+, crosslinking can occur via displacement of the other chloride ligand, typically by another guanine.[11] Cisplatin crosslinks DNA in several different ways, interfering with cell division by mitosis. The damaged DNA elicits DNA repair mechanisms, which in turn activate apoptosis when repair proves impossible. In 2008, researchers were able to show that the apoptosis induced by cisplatin on human colon cancer cells depends on the mitochondrial serine-protease Omi/Htra2.[12] Since this was only demonstrated for colon carcinoma cells, it remains an open question if the Omi/Htra2 protein participates in the cisplatin-induced apoptosis in carcinomas from other tissues.
Most notable among the changes in DNA are the 1,2-intrastrand cross-links with purine bases. These include 1,2-intrastrand d(GpG) adducts which form nearly 90% of the adducts and the less common 1,2-intrastrand d(ApG) adducts. 1,3-intrastrand d(GpXpG) adducts occur but are readily excised by the nucleotide excision repair (NER). Other adducts include inter-strand crosslinks and nonfunctional adducts that have been postulated to contribute to cisplatin's activity. Interaction with cellular proteins, particularly HMG domain proteins, has also been advanced as a mechanism of interfering with mitosis, although this is probably not its primary method of action.
Note that although cisplatin is frequently designated as an alkylating agent, it has no alkyl group and so cannot carry out alkylating reactions. It is correctly classified as alkylating-like.
Cisplatin resistance
Cisplatin combination chemotherapy is the cornerstone of treatment of many cancers. Initial platinum responsiveness is high but the majority of cancer patients will eventually relapse with cisplatin-resistant disease. Many mechanisms of cisplatin resistance have been proposed including changes in cellular uptake and efflux of the drug, increased detoxification of the drug, inhibition of apoptosis and increased DNA repair.[13] Oxaliplatin is active in highly cisplatin-resistant cancer cells in the laboratory; however, there is little evidence for its activity in the clinical treatment of patients with cisplatin-resistant cancer.[13] The drug paclitaxel may be useful in the treatment of cisplatin-resistant cancer; the mechanism for this activity is unknown.[14]
Transplatin
Transplatin, the trans stereoisomer of cisplatin, has formula trans-[PtCl2(NH3)2] and does not exhibit a comparably useful pharmacological effect. Its low activity is generally thought to be due to rapid deactivation of the drug before it can arrive at the DNA.[citation needed] It is toxic, and it is desirable to test batches of cisplatin for the absence of the trans isomer. In a procedure by Woollins et al., which is based on the classic 'Kurnakov test', thiourea reacts with the sample to give derivatives which can easily be separated and detected by HPLC.[15]
History
The compound cis-[Pt(NH3)2(Cl)2] was first described by Michele Peyrone in 1845, and known for a long time as Peyrone's salt.[16] The structure was deduced by Alfred Werner in 1893.[11] In 1965, Barnett Rosenberg, van Camp et al. of Michigan State University discovered that electrolysis of platinum electrodes generated a soluble platinum complex which inhibited binary fission in Escherichia coli (E. coli) bacteria. Although bacterial cell growth continued, cell division was arrested, the bacteria growing as filaments up to 300 times their normal length.[17] The octahedral Pt(IV) complex cis[PtCl4(NH3)2], but not the trans isomer, was found to be effective at forcing filamentous growth of E. coli cells. The square planar Pt(II) complex, cis-[PtCl2(NH3)2] turned out to be even more effective at forcing filamentous growth.[18][19] This finding led to the observation that cis-[PtCl2(NH3)2] was indeed highly effective at regressing the mass of sarcomas in rats.[20] Confirmation of this discovery, and extension of testing to other tumour cell lines launched the medicinal applications of cisplatin. Cisplatin was approved for use in testicular and ovarian cancers by the U.S. Food and Drug Administration on 19 December 1978.,[11][21][22] and in the UK (and in several other European countries) in 1979.[23]
Synthesis
The synthesis of cisplatin starts from potassium tetrachloroplatinate. [24] [25] The tetraiodide is formed by reaction with an excess of potassium iodide. Reaction with ammonia forms K2[PtI2(NH3)2] which is isolated as a yellow compound. When silver nitrate in water is added insoluble silver iodide precipitates and K2[Pt(OH2)2(NH3)2] remains in solution. Addition of potassium chloride will form the final product which precipitates [24] In the triiodo intermediate the addition of the second ammonia ligand is governed by the trans effect. [24]
For the synthesis of transplatin K2[PtCl4] is first converted to Cl2[Pt(NH3)4] by reaction with ammonia. The trans product is then formed by reaction with hydrochloric acid. [24]
See also
- Carboplatin
- Ormaplatin
- Dicycloplatin
- Zeniplatin
References
- ^ Anonymous. Substance Details-Cisplatin. https://scifinder-cas-org.proxy.library.nd.edu/scifinder/view/scifinder/scifinderExplore.jsf (accessed November 13, 2014)
- ^ See also metal amine complex
- ^ Apps, M. G., Choi, E. H. Y., Wheate, N. J. (2015). "The state-of-play and future of platinum drugs". Endocrine-related Cancer 22 (4): 219–233. doi:10.1530/ERC-15-0237. PMID 26113607.
- ^ "www.who.int" (PDF).
- ^ National Cancer Institute. Cisplatin. http://www.cancer.gov/cancertopics/druginfo/cisplatin (accessed November 13, 2014)
- ^ Einhorn LH (1 November 1990). "Treatment of testicular cancer: a new and improved model". J. Clin. Oncol. 8 (11): 1777–81. PMID 1700077.
- ^ Loehrer PJ, Einhorn LH (May 1984). "Drugs five years later. Cisplatin". Annals of Internal Medicine 100 (5): 704–13. doi:10.7326/0003-4819-100-5-704. PMID 6370067.
- ^ a b c Milosavljevic N, Duranton C, Djerbi N, Puech PH, Gounon P, Lagadic-Gossmann D, Dimanche-Boitrel MT, Rauch C, Tauc M, Counillon L, Poët M (2010). "Nongenomic effects of cisplatin: acute inhibition of mechanosensitive transporters and channels without actin remodeling". Cancer Res. 70 (19): 7514–22. doi:10.1158/0008-5472.CAN-10-1253. PMID 20841472. /releases/2010/10/101005141117.htm Lay summary – ScienceDaily.
- ^ Levi JA, Aroney RS, Dalley DN (June 1981). "Haemolytic anaemia after cisplatin treatment". Br Med J (Clin Res Ed) 282 (6281): 2003–4. doi:10.1136/bmj.282.6281.2003. PMC 1505958. PMID 6788166.
- ^ Wang, Dong; Lippard, Stephen J. (2005). "Cellular processing of platinum anticancer drugs". Nature Reviews Drug Discovery 4 (4): 307–320. doi:10.1038/nrd1691. ISSN 1474-1776.
- ^ a b c Stephen Trzaska (20 June 2005). "Cisplatin". C&EN News 83 (25).
- ^ Pruefer FG, Lizarraga F, Maldonado V, Melendez-Zajgla J (June 2008). "Participation of Omi Htra2 serine-protease activity in the apoptosis induced by cisplatin on SW480 colon cancer cells". J Chemother 20 (3): 348–54. doi:10.1179/joc.2008.20.3.348. PMID 18606591.
- ^ a b Stordal B, Davey M (November 2007). "Understanding cisplatin resistance using cellular models". IUBMB Life 59 (11): 696–9. doi:10.1080/15216540701636287. PMID 17885832.
- ^ Stordal B, Pavlakis N, Davey R (December 2007). "A systematic review of platinum and taxane resistance from bench to clinic: an inverse relationship". Cancer Treat. Rev. 33 (8): 688–703. doi:10.1016/j.ctrv.2007.07.013. PMID 17881133.
- ^ Woollins JD, Woollins A, Rosenberg B (1983). "The detection of trace amounts of trans-Pt(NH3)2Cl2 in the presence of cis-Pt(NH3)2Cl2. A high performance liquid chromatographic application of kurnakow's test". Polyhedron 2 (3): 175–178. doi:10.1016/S0277-5387(00)83954-6.
- ^ Peyrone M (1844). "Ueber die Einwirkung des Ammoniaks auf Platinchlorür". Ann Chemie Pharm 51 (1): 1–29. doi:10.1002/jlac.18440510102.
- ^ Rosenberg B, Vancamp L, Krigas T (1965). "Inhibition of cell division in Escherichia coli by electrolysis products from a platinum electrode". Nature 205 (4972): 698–699. doi:10.1038/205698a0. PMID 14287410.
- ^ Rosenberg B, Van Camp L, Grimley EB, Thomson AJ (March 1967). "The inhibition of growth or cell division in Escherichia coli by different ionic species of platinum(IV) complexes". J. Biol. Chem. 242 (6): 1347–52. PMID 5337590.
- ^ Thomson AJ (2007). Christie DA, Tansey EM, eds. "The Discovery, Use and Impact of Platinum Salts as Chemotherapy Agent for Cancer". Wellcome Trust Witnesses to Twentieth Century Medicine 30: 6–15. ISBN 978-0-85484-112-7.
- ^ Rosenberg B, VanCamp L, Trosko JE, Mansour VH (April 1969). "Platinum compounds: a new class of potent antitumour agents". Nature 222 (5191): 385–6. doi:10.1038/222385a0. PMID 5782119.
- ^ Carpenter DP (2010). Reputation and power: organizational image and pharmaceutical regulation at the FDA. Princeton, N.J: Princeton University Press. ISBN 0-691-14180-0.
- ^ "Approval Summary for cisplatin for Metastatic ovarian tumors". FDA Oncology Tools. Food and Drug Administration, Center for Drug Evaluation and Research. 19 December 1978. Archived from the original on 8 February 2008. Retrieved 2009-07-15.
- ^ Wiltshaw E (1979). "Cisplatin in the treatment of cancer". Platinum Metals Review 23 (3): 90–8.
- ^ a b c d The Discovery and Development of Cisplatin Rebecca A. Alderden, Matthew D. Hall and Trevor W. Hambley J. Chem. Educ., 2006, 83 (5), p 728 doi:10.1021/ed083p728
- ^ Dhara, S. C. Indian J. Chem. 1970, 8, 193–134
External links
- Cisplatin: The Invention of an Anticancer Drug by Andri Smith
- Anti-cancer Agents: A treatment of Cisplatin and their analogues by Sia M. Liu (excellent detailed overview)
- MedlinePlus page on cisplatin
- IARC Monograph: "Cisplatin"
- Cisplatinum at The Periodic Table of Videos (University of Nottingham)
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Platinum compounds
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|
| Pt(0) |
|
|
| Pt(II) |
- Pt(NH3)2(CO2)2C4H6
- Pt(NH3)2Cl2
- K2Pt(CN)4
- Pt(NH3)4PtCl4
- Pt(NH3)2CO2CH2O
- C6H10(NH2)2PtC2O4
- NH3PtCl2NC5H4CH3
- Pt(C2H3O2)2
- PtBr2
- PtCl2
- K2PtCl4
- (PtCl(NH3)2C6H12(NH2)2)Pt(NH3)2(NO3)4
- Pt(OH)2
- PtS
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Organoplatinum(II) compounds
|
|
|
|
| Pt(IV) |
- PtO2
- (NH4)2PtCl6
- H2PtCl6
- PtBr4
- PtCl4
- PtF4
- K2PtCl6
- Pt(C2H3O2)2Cl2NH3NH2C6H11
- Na2PtCl6
- Pt(OH)4
- PtS2
- XeFPtF5
|
|
| Pt(V) |
|
|
| Pt(VI) |
|
|
