Jump to content

Cisplatin: Difference between revisions

From Wikipedia, the free encyclopedia
Browse history interactively
← Previous edit
Content deleted Content added
VisualWikitext
OAbot (talk | contribs)
Bots
438,441 edits
m Open access bot: hdl updated in citation with #oabot.
→Synthesis: fix link
 
(16 intermediate revisions by 12 users not shown)
Line 1: Line 1:
{{Short description|Chemical compound and pharmaceutical drug}}
{{Short description|Chemical compound and pharmaceutical drug}}
{{redirect|Cisplatine|the Brazilian province that existed from 1821 to 1828|Cisplatina|the conflict in that province|Cisplatine War}}
{{cs1 config|name-list-style=vanc}}
{{cs1 config|name-list-style=vanc}}
{{Use dmy dates|date=June 2023}}
{{Use dmy dates|date=June 2023}}
Line 9: Line 10:
| type =
| type =
| IUPAC_name = [[Polyhedral symbol|(''SP''-4-2)]]-diamminedichloridoplatinum(II)
| IUPAC_name = [[Polyhedral symbol|(''SP''-4-2)]]-diamminedichloridoplatinum(II)
| image = Cisplatin-stereo.svg
| image = CisplatinTR.svg
| alt =
| alt =
| caption =
| caption =
Line 65: Line 66:
| Cl = 2
| Cl = 2
| Pt = 1
| Pt = 1
| smiles = [NH3+]-[Pt-2](Cl)(Cl)[NH3+]
| smiles = [NH3+][Pt+2](Cl)(Cl)[NH3+]
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/2ClH.2H3N.Pt/h2*1H;2*1H3;/q;;;;+2/p-2
| StdInChI = 1S/2ClH.2H3N.Pt/h2*1H;2*1H3;/q;;;;+2/p-2
Line 79: Line 80:


<!-- History and culture -->
<!-- History and culture -->
Cisplatin was discovered in 1845 and licensed for medical use in 1978 and 1979.<ref name=Fis2006>{{cite book | vauthors = Fischer J, Ganellin CR |title=Analogue-based Drug Discovery |date=2006 |publisher=John Wiley & Sons |isbn=9783527607495|page=513|url=https://books.google.com/books?id=FjKfqkaKkAAC&pg=PA513 |language=en|url-status=live|archive-url=https://web.archive.org/web/20161220163817/https://books.google.ca/books?id=FjKfqkaKkAAC&pg=PA513 |archive-date=20 December 2016}}</ref><ref name=AHFS2016>{{cite web |title=Cisplatin |url= https://www.drugs.com/monograph/cisplatin.html |publisher=The American Society of Health-System Pharmacists|access-date=8 December 2016|url-status=live|archive-url=https://web.archive.org/web/20161221012444/https://www.drugs.com/monograph/cisplatin.html|archive-date=21 December 2016}}</ref> It is on the [[WHO Model List of Essential Medicines|World Health Organization's List of Essential Medicines]].<ref name="WHO21st">{{cite book | vauthors = ((World Health Organization)) | title = World Health Organization model list of essential medicines: 21st list 2019 | year = 2019 | hdl = 10665/325771 | author-link = World Health Organization | publisher = World Health Organization | location = Geneva | id = WHO/MVP/EMP/IAU/2019.06. License: CC BY-NC-SA 3.0 IGO | hdl-access=free }}</ref><ref name="WHO22nd">{{cite book | vauthors = ((World Health Organization)) | title = World Health Organization model list of essential medicines: 22nd list (2021) | year = 2021 | hdl = 10665/345533 | author-link = World Health Organization | publisher = World Health Organization | location = Geneva | id = WHO/MHP/HPS/EML/2021.02 | hdl-access=free }}</ref>
Cisplatin was first reported in 1845 and licensed for medical use in 1978 and 1979.<ref name=Fis2006>{{cite book | vauthors = Fischer J, Ganellin CR |title=Analogue-based Drug Discovery |date=2006 |publisher=John Wiley & Sons |isbn=9783527607495|page=513|url=https://books.google.com/books?id=FjKfqkaKkAAC&pg=PA513 |language=en|url-status=live|archive-url=https://web.archive.org/web/20161220163817/https://books.google.ca/books?id=FjKfqkaKkAAC&pg=PA513 |archive-date=20 December 2016}}</ref><ref name=AHFS2016>{{cite web |title=Cisplatin |url= https://www.drugs.com/monograph/cisplatin.html |publisher=The American Society of Health-System Pharmacists|access-date=8 December 2016|url-status=live|archive-url=https://web.archive.org/web/20161221012444/https://www.drugs.com/monograph/cisplatin.html|archive-date=21 December 2016}}</ref> It is on the [[WHO Model List of Essential Medicines|World Health Organization's List of Essential Medicines]].<ref name="WHO21st">{{cite book | vauthors = ((World Health Organization)) | title = World Health Organization model list of essential medicines: 21st list 2019 | year = 2019 | hdl = 10665/325771 | author-link = World Health Organization | publisher = World Health Organization | location = Geneva | id = WHO/MVP/EMP/IAU/2019.06. License: CC BY-NC-SA 3.0 IGO | hdl-access=free }}</ref><ref name="WHO22nd">{{cite book | vauthors = ((World Health Organization)) | title = World Health Organization model list of essential medicines: 22nd list (2021) | year = 2021 | hdl = 10665/345533 | author-link = World Health Organization | publisher = World Health Organization | location = Geneva | id = WHO/MHP/HPS/EML/2021.02 | hdl-access=free }}</ref>


==Medical use==
==Medical use==
Cisplatin is administered [[intravenously]] as short-term infusion in normal saline for treatment of solid and haematological malignancies. It is used to treat various types of cancers, including [[sarcoma]]s, some [[carcinoma]]s (e.g., [[lung cancer|small cell lung cancer]], [[squamous cell carcinoma of the head and neck]] and [[ovarian cancer]]), [[lymphoma]]s, [[bladder cancer]], [[cervical cancer]],<ref>{{cite web |publisher=[[National Cancer Institute]] |title=Cisplatin |date=2 March 2007 |url=http://www.cancer.gov/cancertopics/druginfo/cisplatin |access-date=2014-11-13 |url-status=live |archive-url=https://web.archive.org/web/20141008032500/http://www.cancer.gov/cancertopics/druginfo/cisplatin |archive-date=8 October 2014 }}</ref> and [[germ cell tumor]]s.
Cisplatin is administered [[intravenously]] as short-term infusion in normal saline for treatment of solid and haematological malignancies. It is used to treat various types of cancers, including [[sarcoma]]s, some [[carcinoma]]s (e.g., [[lung cancer|small cell lung cancer]], [[squamous cell carcinoma of the head and neck]] and [[ovarian cancer]]), [[lymphoma]]s, [[bladder cancer]], [[cervical cancer]],<ref>{{cite web |publisher=[[National Cancer Institute]] |title=Cisplatin |date=2 March 2007 |url=http://www.cancer.gov/cancertopics/druginfo/cisplatin |access-date=2014-11-13 |url-status=live |archive-url=https://web.archive.org/web/20141008032500/http://www.cancer.gov/cancertopics/druginfo/cisplatin |archive-date=8 October 2014 }}</ref> and [[germ cell tumor]]s.


Because of its widespread use, the cure rate for testicular cancer has increased from 10% to 85%.<ref name="Treatment of testicular cancer: a n">{{cite journal | vauthors = Einhorn LH | title = Treatment of testicular cancer: a new and improved model | journal = Journal of Clinical Oncology | volume = 8 | issue = 11 | pages = 1777–81 | date = November 1990 | pmid = 1700077 | doi = 10.1200/JCO.1990.8.11.1777 }}</ref>
The introduction of cisplatin as a standard treatment for testicular cancer improved remission rates from 5-10% before 1974 to 75-85% by 1984.<ref name="Treatment of testicular cancer: a n">{{cite journal | vauthors = Einhorn LH | title = Treatment of testicular cancer: a new and improved model | journal = Journal of Clinical Oncology | volume = 8 | issue = 11 | pages = 1777–81 | date = November 1990 | pmid = 1700077 | doi = 10.1200/JCO.1990.8.11.1777 }}</ref>


==Side effects==
==Side effects==
Cisplatin has a number of side effects that can limit its use:
Cisplatin has a number of side effects that can limit its use:
* [[Nephrotoxicity]] (kidney damage) is the primary dose-limiting side effect and is of major clinical concern. Cisplatin selectively accumulates into the [[proximal tubule]] via basolateral-to-apical transport, where it disrupts mitochondrial energetics and [[endoplasmic reticulum]] Ca<sup>2+</sup> homeostasis and stimulates [[reactive oxygen species]] and pro-inflammatory [[cytokines]].<ref name="Miller">{{cite journal |journal = Toxins |date = October 2010| volume = 2|issue = 11|pages = 2490–2518 | title = Mechanisms of Cisplatin Nephrotoxicity. |vauthors = Miller RP, Tadagavadi RK, Ramesh G, Reeves WB | doi=10.3390/toxins2112490| pmid=22069563 | pmc=3153174 | doi-access=free }}</ref> Multiple mitigation strategies are being explored clinically and pre-clinically, including hydration regimens, [[amifostine]], transporter inhibitors, antioxidants, anti-inflammatories, and [[epoxyeicosatrienoic acids]] and their analogues.<ref name=Miller/><ref name="Singh">{{cite journal |journal= Chemical Research in Toxicology |date =November 2021| volume=34|issue=12|pages=2579–2591 | title= New Alkoxy- Analogues of Epoxyeicosatrienoic Acids Attenuate Cisplatin Nephrotoxicity In Vitro via Reduction of Mitochondrial Dysfunction, Oxidative Stress, Mitogen-Activated Protein Kinase Signaling, and Caspase Activation. |vauthors=Singh N, Vik A, Lybrand DB, Morisseau C, Hammock BD | doi=10.1021/acs.chemrestox.1c00347|pmid =34817988|pmc =8853703}}</ref>
* [[Nephrotoxicity]] (kidney damage) is the primary dose-limiting side effect and is of major clinical concern. Cisplatin selectively accumulates into the [[proximal tubule]] via basolateral-to-apical transport, where it disrupts mitochondrial energetics and [[endoplasmic reticulum]] Ca<sup>2+</sup> homeostasis and stimulates [[reactive oxygen species]] and pro-inflammatory [[cytokines]].<ref name="Miller">{{cite journal |journal = Toxins |date = October 2010| volume = 2|issue = 11|pages = 2490–2518 | title = Mechanisms of Cisplatin Nephrotoxicity. |vauthors = Miller RP, Tadagavadi RK, Ramesh G, Reeves WB | doi=10.3390/toxins2112490| pmid=22069563 | pmc=3153174 | doi-access=free }}</ref> Multiple mitigation strategies are being explored clinically and pre-clinically, including hydration regimens, [[amifostine]], transporter inhibitors, antioxidants, anti-inflammatories, and [[epoxyeicosatrienoic acids]] and their analogues.<ref name=Miller/><ref name="Singh">{{cite journal |journal= Chemical Research in Toxicology |date =November 2021| volume=34|issue=12|pages=2579–2591 | title= New Alkoxy- Analogues of Epoxyeicosatrienoic Acids Attenuate Cisplatin Nephrotoxicity In Vitro via Reduction of Mitochondrial Dysfunction, Oxidative Stress, Mitogen-Activated Protein Kinase Signaling, and Caspase Activation. |vauthors=Singh N, Vik A, Lybrand DB, Morisseau C, Hammock BD | doi=10.1021/acs.chemrestox.1c00347|pmid =34817988|pmc =8853703}}</ref>
* [[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.<ref name="Milosavljevic_2010">{{cite journal | vauthors = Milosavljevic N, Duranton C, Djerbi N, Puech PH, Gounon P, Lagadic-Gossmann D, Dimanche-Boitrel MT, Rauch C, Tauc M, Counillon L, Poët M | display-authors = 6 | title = Nongenomic effects of cisplatin: acute inhibition of mechanosensitive transporters and channels without actin remodeling | journal = Cancer Research | volume = 70 | issue = 19 | pages = 7514–22 | date = October 2010 | pmid = 20841472 | doi = 10.1158/0008-5472.CAN-10-1253 | url = https://www.sciencedaily.com/releases/2010/10/101005141117.htm | doi-access = free }}</ref> 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 [[SLC9A1|NHE-1]].<ref name="Milosavljevic_2010"/> 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&nbsp;μg/mL) and reversible.<ref name="Milosavljevic_2010"/> Cisplatin can increase levels of [[sphingosine-1-phosphate]] in the [[central nervous system]], contributing to the development of [[post-chemotherapy cognitive impairment]].<ref name="pmid36047496">{{cite journal |vauthors=Squillace S, Niehoff ML, Doyle TM, Green M, Esposito E, Cuzzocrea S, Arnatt CK, Spiegel S, Farr SA, Salvemini D |title=Sphingosine-1-phosphate receptor 1 activation in the central nervous system drives cisplatin-induced cognitive impairment |journal=The Journal of Clinical Investigation |volume=132 |issue=17 |date=September 2022 |pmid=36047496 |pmc=9433103 |doi=10.1172/JCI157738}}</ref><ref>{{cite web|url= https://neurosciencenews.com/chemo-brain-drug-21353/|title=Unlocking the Mystery of "Chemo Brain" | work = Neuroscience News |date=2 September 2022}}</ref>
* [[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.<ref name="Milosavljevic_2010">{{cite journal | vauthors = Milosavljevic N, Duranton C, Djerbi N, Puech PH, Gounon P, Lagadic-Gossmann D, Dimanche-Boitrel MT, Rauch C, Tauc M, Counillon L, Poët M | display-authors = 6 | title = Nongenomic effects of cisplatin: acute inhibition of mechanosensitive transporters and channels without actin remodeling | journal = Cancer Research | volume = 70 | issue = 19 | pages = 7514–22 | date = October 2010 | pmid = 20841472 | doi = 10.1158/0008-5472.CAN-10-1253 | url = https://www.sciencedaily.com/releases/2010/10/101005141117.htm | doi-access = free }}</ref> 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. Cisplatin noncompetitively inhibits an archetypal, membrane-bound mechanosensitive sodium-hydrogen ion transporter known as [[SLC9A1|NHE-1]].<ref name="Milosavljevic_2010"/> 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&nbsp;μg/mL) and reversible.<ref name="Milosavljevic_2010"/> Cisplatin can increase levels of [[sphingosine-1-phosphate]] in the [[central nervous system]], contributing to the development of [[post-chemotherapy cognitive impairment]].<ref name="pmid36047496">{{cite journal |vauthors=Squillace S, Niehoff ML, Doyle TM, Green M, Esposito E, Cuzzocrea S, Arnatt CK, Spiegel S, Farr SA, Salvemini D |title=Sphingosine-1-phosphate receptor 1 activation in the central nervous system drives cisplatin-induced cognitive impairment |journal=The Journal of Clinical Investigation |volume=132 |issue=17 |date=September 2022 |pmid=36047496 |pmc=9433103 |doi=10.1172/JCI157738}}</ref><ref>{{cite web|url= https://neurosciencenews.com/chemo-brain-drug-21353/|title=Unlocking the Mystery of "Chemo Brain" | work = Neuroscience News |date=2 September 2022}}</ref>
* [[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]].
* [[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]] and hearing loss associated with cisplatin can be severe and is considered to be a dose-limiting side effect.<ref name="pmid29051464"/> 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]]. In September 2022, the U.S. [[Food and Drug Administration]] (FDA) approved [[Sodium thiosulfate (medical use)|sodium thiosulfate]] under the brand name Pedmark to lessen the risk of ototoxicity and hearing loss in people receiving cisplatin.<ref name="pmid35489339">{{cite journal |vauthors=Orgel E, Villaluna D, Krailo MD, Esbenshade A, Sung L, Freyer DR |title=Sodium thiosulfate for prevention of cisplatin-induced hearing loss: updated survival from ACCL0431 |journal=The Lancet. Oncology |volume=23 |issue=5 |pages=570–572 |date=May 2022 |pmid=35489339 |pmc=9635495 |doi=10.1016/S1470-2045(22)00155-3}}</ref><ref name="Winstead 2022">{{cite web | vauthors = Winstead E |title=Sodium Thiosulfate Reduces Hearing Loss in Kids with Cancer |website=National Cancer Institute |date=6 October 2022 |url=https://www.cancer.gov/news-events/cancer-currents-blog/2022/fda-sodium-thiosulfate-cisplatin-hearing-loss-children |access-date=9 March 2023}}</ref><ref name="FDA 2022">{{cite web |title=FDA approves sodium thiosulfate to reduce the risk of ototoxicity associated with cisplatin in pediatric patients with localized, non-metastatic solid tumors |publisher=Food and Drug Administration |date=20 September 2022 |url=https://www.fda.gov/drugs/resources-information-approved-drugs/fda-approves-sodium-thiosulfate-reduce-risk-ototoxicity-associated-cisplatin-pediatric-patients |access-date=9 March 2023}}</ref> There is ongoing investigation of [[acetylcysteine]] injections as a preventative measure.<ref name="pmid29051464"/><ref>{{cite journal | vauthors = Sarafraz Z, Ahmadi A, Daneshi A | title = Transtympanic Injections of N-acetylcysteine and Dexamethasone for Prevention of Cisplatin-Induced Ototoxicity: Double Blind Randomized Clinical Trial | journal = The International Tinnitus Journal | volume = 22 | issue = 1 | pages = 40–45 | date = June 2018 | pmid = 29993216 | doi = 10.5935/0946-5448.20180007 }}</ref>
* [[Ototoxicity]] and hearing loss associated with cisplatin can be severe and is considered to be a dose-limiting side effect.<ref name="pmid29051464"/> 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]]. In September 2022, the U.S. [[Food and Drug Administration]] (FDA) approved [[Sodium thiosulfate (medical use)|sodium thiosulfate]] under the brand name Pedmark to lessen the risk of ototoxicity and hearing loss in people receiving cisplatin.<ref name="pmid35489339">{{cite journal |vauthors=Orgel E, Villaluna D, Krailo MD, Esbenshade A, Sung L, Freyer DR |title=Sodium thiosulfate for prevention of cisplatin-induced hearing loss: updated survival from ACCL0431 |journal=The Lancet. Oncology |volume=23 |issue=5 |pages=570–572 |date=May 2022 |pmid=35489339 |pmc=9635495 |doi=10.1016/S1470-2045(22)00155-3}}</ref><ref name="Winstead 2022">{{cite web | vauthors = Winstead E |title=Sodium Thiosulfate Reduces Hearing Loss in Kids with Cancer |website=National Cancer Institute |date=6 October 2022 |url=https://www.cancer.gov/news-events/cancer-currents-blog/2022/fda-sodium-thiosulfate-cisplatin-hearing-loss-children |access-date=9 March 2023}}</ref><ref name="FDA 2022">{{cite web |title=FDA approves sodium thiosulfate to reduce the risk of ototoxicity associated with cisplatin in pediatric patients with localized, non-metastatic solid tumors |publisher=Food and Drug Administration |date=20 September 2022 |url=https://www.fda.gov/drugs/resources-information-approved-drugs/fda-approves-sodium-thiosulfate-reduce-risk-ototoxicity-associated-cisplatin-pediatric-patients |access-date=9 March 2023}}</ref> There is ongoing investigation of [[acetylcysteine]] injections as a preventative measure.<ref name="pmid29051464"/><ref>{{cite journal | vauthors = Sarafraz Z, Ahmadi A, Daneshi A | title = Transtympanic Injections of N-acetylcysteine and Dexamethasone for Prevention of Cisplatin-Induced Ototoxicity: Double Blind Randomized Clinical Trial | journal = The International Tinnitus Journal | volume = 22 | issue = 1 | pages = 40–45 | date = June 2018 | pmid = 29993216 | doi = 10.5935/0946-5448.20180007 }}</ref>
Line 100: Line 101:
The water molecule in ''cis''-[PtCl(NH<sub>3</sub>)<sub>2</sub>(H<sub>2</sub>O)]<sup>+</sup> is itself easily displaced by the ''N''-[[Heterocyclic amine|heterocyclic base]]s on [[DNA]]. [[Guanine]] preferentially binds. A model compound has been prepared and crystals were examined by [[X-ray]] crystallography<ref>{{cite journal | vauthors = Orbell JD, Solorzano C, Marzilli LG, Kistenmacher TJ | title = Preparation and structure of cis-chlorodiammine (N2, N2-dimethyl-9-methylguanine) platinum (II) hexafluorophosphate. A model for the intermediate in the proposed crosslinking mode of action of platinum (II) antitumor agents. | journal = Inorganic Chemistry | date = October 1982 | volume = 21 | issue = 10 | pages = 3806–3810 | doi = 10.1021/ic00140a041 }}</ref>
The water molecule in ''cis''-[PtCl(NH<sub>3</sub>)<sub>2</sub>(H<sub>2</sub>O)]<sup>+</sup> is itself easily displaced by the ''N''-[[Heterocyclic amine|heterocyclic base]]s on [[DNA]]. [[Guanine]] preferentially binds. A model compound has been prepared and crystals were examined by [[X-ray]] crystallography<ref>{{cite journal | vauthors = Orbell JD, Solorzano C, Marzilli LG, Kistenmacher TJ | title = Preparation and structure of cis-chlorodiammine (N2, N2-dimethyl-9-methylguanine) platinum (II) hexafluorophosphate. A model for the intermediate in the proposed crosslinking mode of action of platinum (II) antitumor agents. | journal = Inorganic Chemistry | date = October 1982 | volume = 21 | issue = 10 | pages = 3806–3810 | doi = 10.1021/ic00140a041 }}</ref>


Subsequent to formation of [PtCl(guanine-DNA)(NH<sub>3</sub>)<sub>2</sub>]<sup>+</sup>, crosslinking can occur via displacement of the other chloride, typically by another guanine.<ref name = trzaska/> 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 [[HTRA2|Omi/Htra2]].<ref name="pmid18606591">{{cite journal |vauthors=Pruefer FG, Lizarraga F, Maldonado V, Melendez-Zajgla J | s2cid = 11052459 | title = Participation of Omi Htra2 serine-protease activity in the apoptosis induced by cisplatin on SW480 colon cancer cells | journal = Journal of Chemotherapy | volume = 20 | issue = 3 | pages = 348–354 | date = June 2008 | pmid = 18606591 | doi = 10.1179/joc.2008.20.3.348 }}</ref> Since this was only demonstrated for colon carcinoma cells, it remains an open question whether the Omi/Htra2 protein participates in the cisplatin-induced apoptosis in carcinomas from other tissues.<ref name="pmid18606591"/>
Subsequent to formation of [PtCl(guanine-DNA)(NH<sub>3</sub>)<sub>2</sub>]<sup>+</sup>, crosslinking can occur via displacement of the other chloride, typically by another guanine.<ref name = trzaska/> Cisplatin crosslinks DNA in several 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, apoptosis induced by cisplatin on human colon cancer cells was shown to depend on the mitochondrial serine-protease [[HTRA2|Omi/Htra2]].<ref name="pmid18606591">{{cite journal |vauthors=Pruefer FG, Lizarraga F, Maldonado V, Melendez-Zajgla J | s2cid = 11052459 | title = Participation of Omi Htra2 serine-protease activity in the apoptosis induced by cisplatin on SW480 colon cancer cells | journal = Journal of Chemotherapy | volume = 20 | issue = 3 | pages = 348–354 | date = June 2008 | pmid = 18606591 | doi = 10.1179/joc.2008.20.3.348 }}</ref> Since this was only demonstrated for colon carcinoma cells, it remains an open question whether the Omi/Htra2 protein participates in the cisplatin-induced apoptosis in carcinomas from other tissues.<ref name="pmid18606591"/>


Most notable among the changes in DNA are the 1,2-intrastrand cross-links with [[purine]] bases. These include 1,2-intrastrand d([[guanine|Gp]]G) adducts, which form nearly 90% of the adducts, and the less common 1,2-intrastrand d([[adenosine|Ap]]G) adducts. Coordination chemists have obtained crystals of the products of reacting cisplain with small models of DNA. Here is a [[POVray]] plot of the platinum binding to a small model of DNA.<ref name="pmid4048939">{{cite journal | vauthors = Sherman SE, Gibson D, Wang AH, Lippard SJ | title = X-ray structure of the major adduct of the anticancer drug cisplatin with DNA: cis-[Pt(NH3)2(d(pGpG))] | journal = Science | volume = 230 | issue = 4724 | pages = 412–7 | date = October 1985 | pmid = 4048939 | doi = 10.1126/science.4048939 | bibcode = 1985Sci...230..412S }}</ref>
Most notable among the changes in DNA are the 1,2-intrastrand cross-links with [[purine]] bases. These include 1,2-intrastrand d([[guanine|Gp]]G) adducts, which form nearly 90% of the adducts, and the less common 1,2-intrastrand d([[adenosine|Ap]]G) adducts. Coordination chemists have obtained crystals of the products of reacting cisplain with small models of DNA. Here is a [[POVray]] plot of the platinum binding to a small model of DNA.<ref name="pmid4048939">{{cite journal | vauthors = Sherman SE, Gibson D, Wang AH, Lippard SJ | title = X-ray structure of the major adduct of the anticancer drug cisplatin with DNA: cis-[Pt(NH3)2(d(pGpG))] | journal = Science | volume = 230 | issue = 4724 | pages = 412–7 | date = October 1985 | pmid = 4048939 | doi = 10.1126/science.4048939 | bibcode = 1985Sci...230..412S }}</ref>
Line 109: Line 110:


=== Cisplatin resistance ===
=== 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]] , increased [[DNA repair]] or changes in metabolism <ref>{{cite journal |last1=Cruz-Bermúdez |first1=Alberto |last2=Laza-Briviesca |first2=Raquel |last3=Vicente-Blanco |first3=Ramiro J. |last4=García-Grande |first4=Aránzazu |last5=Coronado |first5=Maria José |last6=Laine-Menéndez |first6=Sara |last7=Palacios-Zambrano |first7=Sara |last8=Moreno-Villa |first8=M. Rocío |last9=Ruiz-Valdepeñas |first9=Asunción Martin |last10=Lendinez |first10=Cristina |last11=Romero |first11=Atocha |last12=Franco |first12=Fernando |last13=Calvo |first13=Virginia |last14=Alfaro |first14=Cristina |last15=Acosta |first15=Paloma Martin |last16=Salas |first16=Clara |last17=Garcia |first17=José Miguel |last18=Provencio |first18=Mariano |title=Cisplatin resistance involves a metabolic reprogramming through ROS and PGC-1α in NSCLC which can be overcome by OXPHOS inhibition |journal=Free Radical Biology and Medicine |date=May 2019 |volume=135 |pages=167–181 |doi=10.1016/j.freeradbiomed.2019.03.009|hdl=10486/688357 |hdl-access=free }}</ref>.<ref name="Stordal_2007">{{cite journal | vauthors = Stordal B, Davey M | title = Understanding cisplatin resistance using cellular models | journal = IUBMB Life | volume = 59 | issue = 11 | pages = 696–699 | date = November 2007 | pmid = 17885832 | doi = 10.1080/15216540701636287 | s2cid = 30879019 | url = http://doras.dcu.ie/2202/1/Stordal-IUBMB-2007.pdf | doi-access = free }}</ref> [[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.<ref name="Stordal_2007"/> The drug [[paclitaxel]] may be useful in the treatment of cisplatin-resistant cancer; the mechanism for this activity is as yet unknown.<ref name="pmid17881133">{{cite journal | vauthors = Stordal B, Pavlakis N, Davey R | title = A systematic review of platinum and taxane resistance from bench to clinic: an inverse relationship | journal = Cancer Treatment Reviews | volume = 33 | issue = 8 | pages = 688–703 | date = December 2007 | pmid = 17881133 | doi = 10.1016/j.ctrv.2007.07.013 | url = http://doras.dcu.ie/2190/1/StordalCTR2007-Paclitaxel.pdf | hdl = 2123/4068 }}</ref>
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]], increased [[DNA repair]] or changes in metabolism.<ref>{{cite journal | vauthors = Cruz-Bermúdez A, Laza-Briviesca R, Vicente-Blanco RJ, García-Grande A, Coronado MJ, Laine-Menéndez S, Palacios-Zambrano S, Moreno-Villa MR, Ruiz-Valdepeñas AM, Lendinez C, Romero A, Franco F, Calvo V, Alfaro C, Acosta PM, Salas C, Garcia JM, Provencio M | display-authors = 6 | title = Cisplatin resistance involves a metabolic reprogramming through ROS and PGC-1α in NSCLC which can be overcome by OXPHOS inhibition | journal = Free Radical Biology & Medicine | volume = 135 | pages = 167–181 | date = May 2019 | pmid = 30880247 | doi = 10.1016/j.freeradbiomed.2019.03.009 | hdl-access = free | hdl = 10486/688357 }}</ref><ref name="Stordal_2007">{{cite journal | vauthors = Stordal B, Davey M | title = Understanding cisplatin resistance using cellular models | journal = IUBMB Life | volume = 59 | issue = 11 | pages = 696–699 | date = November 2007 | pmid = 17885832 | doi = 10.1080/15216540701636287 | s2cid = 30879019 | url = http://doras.dcu.ie/2202/1/Stordal-IUBMB-2007.pdf | doi-access = free }}</ref> [[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.<ref name="Stordal_2007"/> The drug [[paclitaxel]] may be useful in the treatment of cisplatin-resistant cancer; the mechanism for this activity is as yet unknown.<ref name="pmid17881133">{{cite journal | vauthors = Stordal B, Pavlakis N, Davey R | title = A systematic review of platinum and taxane resistance from bench to clinic: an inverse relationship | journal = Cancer Treatment Reviews | volume = 33 | issue = 8 | pages = 688–703 | date = December 2007 | pmid = 17881133 | doi = 10.1016/j.ctrv.2007.07.013 | url = http://doras.dcu.ie/2190/1/StordalCTR2007-Paclitaxel.pdf | hdl = 2123/4068 }}</ref>


===Transplatin===
===Transplatin===
Line 129: Line 130:
Cisplatin was the first to be developed.<ref name=Kelland>{{cite journal | vauthors = Kelland L | title = The resurgence of platinum-based cancer chemotherapy | doi = 10.1038/nrc2167 | journal = Nature Reviews Cancer | volume = 7 | issue = 8 | pages = 573–584 | year = 2007 | pmid = 17625587| s2cid = 205468214 }}</ref>
Cisplatin was the first to be developed.<ref name=Kelland>{{cite journal | vauthors = Kelland L | title = The resurgence of platinum-based cancer chemotherapy | doi = 10.1038/nrc2167 | journal = Nature Reviews Cancer | volume = 7 | issue = 8 | pages = 573–584 | year = 2007 | pmid = 17625587| s2cid = 205468214 }}</ref>
In 1983 pediatric oncologist Roger Packer began incorporating cisplatin into adjuvant chemotherapy for the treatment of childhood [[medulloblastoma]].<ref>{{cite journal | vauthors = Packer RJ, Sutton LN, Elterman R, Lange B, Goldwein J, Nicholson HS, Mulne L, Boyett J, D'Angio G, Wechsler-Jentzsch K | display-authors = 6 | title = Outcome for children with medulloblastoma treated with radiation and cisplatin, CCNU, and vincristine chemotherapy | journal = Journal of Neurosurgery | volume = 81 | issue = 5 | pages = 690–8 | date = November 1994 | pmid = 7931615 | doi = 10.3171/jns.1994.81.5.0690 }}</ref> The new protocol that he developed led to a marked increase in disease-free survival rates for patients with medulloblastoma, up to around 85%.<ref>{{cite journal | vauthors = Packer RJ, Sutton LN, Goldwein JW, Perilongo G, Bunin G, Ryan J, Cohen BH, D'Angio G, Kramer ED, Zimmerman RA | display-authors = 6 | title = Improved survival with the use of adjuvant chemotherapy in the treatment of medulloblastoma | journal = Journal of Neurosurgery | volume = 74 | issue = 3 | pages = 433–40 | date = March 1991 | pmid = 1847194 | doi = 10.3171/jns.1991.74.3.0433 }}</ref> The Packer Protocol has since become a standard treatment for medulloblastoma. Likewise, cisplatin has been found to be particularly effective against [[testicular cancer]], where its use improved the cure rate from 10% to 85%.<ref name="Treatment of testicular cancer: a n"/>
In 1983 pediatric oncologist Roger Packer began incorporating cisplatin into adjuvant chemotherapy for the treatment of childhood [[medulloblastoma]].<ref>{{cite journal | vauthors = Packer RJ, Sutton LN, Elterman R, Lange B, Goldwein J, Nicholson HS, Mulne L, Boyett J, D'Angio G, Wechsler-Jentzsch K | display-authors = 6 | title = Outcome for children with medulloblastoma treated with radiation and cisplatin, CCNU, and vincristine chemotherapy | journal = Journal of Neurosurgery | volume = 81 | issue = 5 | pages = 690–8 | date = November 1994 | pmid = 7931615 | doi = 10.3171/jns.1994.81.5.0690 }}</ref> The new protocol that he developed led to a marked increase in disease-free survival rates for patients with medulloblastoma, up to around 85%.<ref>{{cite journal | vauthors = Packer RJ, Sutton LN, Goldwein JW, Perilongo G, Bunin G, Ryan J, Cohen BH, D'Angio G, Kramer ED, Zimmerman RA | display-authors = 6 | title = Improved survival with the use of adjuvant chemotherapy in the treatment of medulloblastoma | journal = Journal of Neurosurgery | volume = 74 | issue = 3 | pages = 433–40 | date = March 1991 | pmid = 1847194 | doi = 10.3171/jns.1991.74.3.0433 }}</ref> The Packer Protocol has since become a standard treatment for medulloblastoma. Likewise, cisplatin has been found to be particularly effective against [[testicular cancer]], where its use improved the cure rate from 10% to 85%.<ref name="Treatment of testicular cancer: a n"/>

Recently, some researchers have investigated at the preclinical level new forms of cisplatin [[prodrug]]s in combination with [[nanomaterials]] in order to localize the release of the [[drug]] in the target.<ref>{{cite journal | vauthors = Dhar S, Daniel WL, Giljohann DA, Mirkin CA, Lippard SJ | title = Polyvalent oligonucleotide gold nanoparticle conjugates as delivery vehicles for platinum(IV) warheads | journal = Journal of the American Chemical Society | volume = 131 | issue = 41 | pages = 14652–3 | date = October 2009 | pmid = 19778015 | pmc = 2761975 | doi = 10.1021/ja9071282 }}</ref><ref>{{cite journal | vauthors = Santi M, Mapanao AK, Cassano D, Vlamidis Y, Cappello V, Voliani V | title = Endogenously-Activated Ultrasmall-in-Nano Therapeutics: Assessment on 3D Head and Neck Squamous Cell Carcinomas | journal = Cancers | volume = 12 | issue = 5 | pages = 1063 | date = April 2020 | pmid = 32344838 | pmc = 7281743 | doi = 10.3390/cancers12051063 | doi-access = free }}</ref>


==Synthesis==
==Synthesis==
Syntheses of cisplatin start from [[potassium tetrachloroplatinate]]. Several procedures are available. One obstacle is the facile formation of [[Magnus's green salt]] (MGS), which has the same empirical formula as cisplatin. The traditional way to avoid MGS involves the conversion of K<sub>2</sub>PtCl<sub>4</sub> to K<sub>2</sub>PtI<sub>4</sub>, as originally described by Dhara.<ref>{{cite journal|title=Cisplatin| vauthors = Dhara SC |journal=Indian J. Chem. |date=1970|volume= 8|pages= 123–134}}</ref><ref name=Alderden>{{cite journal|title=The Discovery and Development of Cisplatin| vauthors = Alderden RA, Hall MD, Hambley TW |s2cid= 29546931 |journal=[[J. Chem. Educ.]]|date= 2006|volume= 83 |issue=5 |page=728 |doi=10.1021/ed083p728|bibcode=2006JChEd..83..728A}}</ref> Reaction with [[ammonia]] forms PtI<sub>2</sub>(NH<sub>3</sub>)<sub>2</sub> which is isolated as a yellow compound. When [[silver nitrate]] in water is added insoluble [[silver iodide]] precipitates and [Pt(OH<sub>2</sub>)<sub>2</sub>(NH<sub>3</sub>)<sub>2</sub>](NO<sub>3</sub>)<sub>2</sub> remains in solution. Addition of [[potassium chloride]] will form the final product which precipitates<ref name=Alderden /> In the triiodo intermediate the addition of the second ammonia ligand is governed by the [[trans effect]].<ref name=Alderden />
Syntheses of cisplatin start from [[potassium tetrachloroplatinate]]. Several procedures are available. One obstacle is the facile formation of [[Magnus's green salt]] (MGS), which has the same empirical formula as cisplatin. The traditional way to avoid MGS involves the conversion of K<sub>2</sub>PtCl<sub>4</sub> to [[Potassium tetraiodoplatinate|K<sub>2</sub>PtI<sub>4</sub>]], as originally described by Dhara.<ref>{{cite journal|title=Cisplatin| vauthors = Dhara SC |journal=Indian J. Chem. |date=1970|volume= 8|pages= 123–134}}</ref><ref name=Alderden>{{cite journal|title=The Discovery and Development of Cisplatin| vauthors = Alderden RA, Hall MD, Hambley TW |s2cid= 29546931 |journal=[[J. Chem. Educ.]]|date= 2006|volume= 83 |issue=5 |page=728 |doi=10.1021/ed083p728|bibcode=2006JChEd..83..728A}}</ref> Reaction with [[ammonia]] forms PtI<sub>2</sub>(NH<sub>3</sub>)<sub>2</sub> which is isolated as a yellow compound. When [[silver nitrate]] in water is added insoluble [[silver iodide]] precipitates and [Pt(OH<sub>2</sub>)<sub>2</sub>(NH<sub>3</sub>)<sub>2</sub>](NO<sub>3</sub>)<sub>2</sub> remains in solution. Addition of [[potassium chloride]] will form the final product which precipitates<ref name=Alderden /> In the triiodo intermediate the addition of the second ammonia ligand is governed by the [[trans effect]].<ref name=Alderden />


:[[File:Cisplatin synthesis.svg|600px]]
:[[File:Cisplatin synthesis.svg|600px]]
Line 141: Line 140:


== Research ==
== Research ==
Cisplatin has been studied with [[Auger therapy]] to increase the therapeutic effects of cisplatin, without increasing normal tissue toxicities.<ref>{{cite journal | vauthors = Ku A, Facca VJ, Cai Z, Reilly RM | title = Auger electrons for cancer therapy - a review | journal = EJNMMI Radiopharmacy and Chemistry | volume = 4 | issue = 1 | pages = 27 | date = October 2019 | pmid = 31659527 | pmc = 6800417 | doi = 10.1186/s41181-019-0075-2 | doi-access = free }}</ref> However, due to significant side effects, the search for structurally novel Pt(II) and Pd(II) compounds exhibiting antineoplastic activity is extremely important and aims to develop more effective and less toxic drugs.<ref>{{cite journal | vauthors = Fiuza SM, Amado AM, Oliveira PJ, Sardão VA, De Carvalho LB, Marques MP |title=Pt(II) vs Pd(II) Polyamine Complexes as New Anticancer Drugs: A Structure- Activity Study |url=https://www.eurekaselect.com/article/1846 |journal=Letters in Drug Design & Discovery |date=2006 |language=en |volume=3 |issue=3 |pages=149–151 |doi=10.2174/157018006776286989|hdl=10316/45139 |hdl-access=free }}</ref> Metal complexes comprising cisplatin-like molecules ([PtCl(NH<sub>3</sub>)<sub>2</sub>] or [Pt(NH<sub>3</sub>)Cl<sub>2</sub>]) linked by variable length alkandiamine chains have attracted great interest in the last few years as next-generation alternatives drugs in cancer chemotherapy.<ref>{{cite journal | vauthors = Teixeira LJ, Seabra M, Reis E, da Cruz MT, de Lima MC, Pereira E, Miranda MA, Marques MP | display-authors = 6 | title = Cytotoxic activity of metal complexes of biogenic polyamines: polynuclear platinum(II) chelates | journal = Journal of Medicinal Chemistry | volume = 47 | issue = 11 | pages = 2917–2925 | date = May 2004 | pmid = 15139770 | doi = 10.1021/jm0311238 | hdl = 10316/10605 | hdl-access = free }}</ref><ref>{{cite journal | vauthors = Vinci D, Chateigner D |date=2022-12-01 |title=Synthesis and structural characterization of a new dinuclear platinum(III) complex, [Pt 2 Cl 4 (NH 3 ) 2 {μ-HN=C(O)Bu t } 2 ] |url=https://scripts.iucr.org/cgi-bin/paper?S2052520622009660 |journal=Acta Crystallographica Section B Structural Science, Crystal Engineering and Materials |volume=78 |issue=6 |pages=835–841 |doi=10.1107/S2052520622009660 |issn=2052-5206 |pmc=9728019}}</ref><ref>{{cite journal | vauthors = Omondi RO, Ojwach SO, Jaganyi D |date= November 2020 |title=Review of comparative studies of cytotoxic activities of Pt(II), Pd(II), Ru(II)/(III) and Au(III) complexes, their kinetics of ligand substitution reactions and DNA/BSA interactions |journal=Inorganica Chimica Acta |language=en |volume=512 |pages=119883 |doi=10.1016/j.ica.2020.119883|s2cid= 225575546 }}</ref>
Cisplatin has been studied with [[Auger therapy]] to increase the therapeutic effects of cisplatin, without increasing normal tissue toxicities.<ref>{{cite journal | vauthors = Ku A, Facca VJ, Cai Z, Reilly RM | title = Auger electrons for cancer therapy - a review | journal = EJNMMI Radiopharmacy and Chemistry | volume = 4 | issue = 1 | pages = 27 | date = October 2019 | pmid = 31659527 | pmc = 6800417 | doi = 10.1186/s41181-019-0075-2 | doi-access = free }}</ref> However, due to significant side effects, the search for structurally novel Pt(II) and Pd(II) compounds exhibiting antineoplastic activity is extremely important and aims to develop more effective and less toxic drugs.<ref>{{cite journal | vauthors = Fiuza SM, Amado AM, Oliveira PJ, Sardão VA, De Carvalho LB, Marques MP |title=Pt(II) vs Pd(II) Polyamine Complexes as New Anticancer Drugs: A Structure- Activity Study |url=https://www.eurekaselect.com/article/1846 |journal=Letters in Drug Design & Discovery |date=2006 |language=en |volume=3 |issue=3 |pages=149–151 |doi=10.2174/157018006776286989|hdl=10316/45139 |hdl-access=free }}</ref> Cisplatin-like molecules ([PtCl(NH<sub>3</sub>)<sub>2</sub>] and [Pt(NH<sub>3</sub>)Cl<sub>2</sub>]) linked by variable length alkandiamine chains have attracted some interest in cancer chemotherapy.<ref>{{cite journal | vauthors = Teixeira LJ, Seabra M, Reis E, da Cruz MT, de Lima MC, Pereira E, Miranda MA, Marques MP | display-authors = 6 | title = Cytotoxic activity of metal complexes of biogenic polyamines: polynuclear platinum(II) chelates | journal = Journal of Medicinal Chemistry | volume = 47 | issue = 11 | pages = 2917–2925 | date = May 2004 | pmid = 15139770 | doi = 10.1021/jm0311238 | hdl = 10316/10605 | hdl-access = free }}</ref><ref>{{cite journal | vauthors = Vinci D, Chateigner D |date=2022-12-01 |title=Synthesis and structural characterization of a new dinuclear platinum(III) complex, [Pt 2 Cl 4 (NH 3 ) 2 {μ-HN=C(O)Bu t } 2 ] |url=https://scripts.iucr.org/cgi-bin/paper?S2052520622009660 |journal=Acta Crystallographica Section B Structural Science, Crystal Engineering and Materials |volume=78 |issue=6 |pages=835–841 |doi=10.1107/S2052520622009660 |issn=2052-5206 |pmc=9728019}}</ref><ref>{{cite journal | vauthors = Omondi RO, Ojwach SO, Jaganyi D |date= November 2020 |title=Review of comparative studies of cytotoxic activities of Pt(II), Pd(II), Ru(II)/(III) and Au(III) complexes, their kinetics of ligand substitution reactions and DNA/BSA interactions |journal=Inorganica Chimica Acta |language=en |volume=512 |pages=119883 |doi=10.1016/j.ica.2020.119883|s2cid= 225575546 }}</ref>


== References ==
== References ==
Line 148: Line 147:
== Further reading ==
== Further reading ==
{{refbegin}}
{{refbegin}}
* {{cite book |last1=Dabrowiak |first1=James C. |chapter = Cisplatin |title=Metals in Medicine |date= 2009 |isbn=978-0-470-68196-1 |edition=1 |doi=10.1002/9780470684986.ch3 | pages =73–107 |publisher= John Wiley & Sons|language=en}}
* {{cite book | vauthors = Riddell IA, Lippard SJ | veditors = Sigel A, Sigel H, Freisinger E, Sigel RK | title = Metallo-Drugs: Development and Action of Anticancer Agents | series = Metal Ions in Life Sciences | volume = 18 | date = 2018 | publisher = de Gruyter GmbH | location = Berlin | isbn = 978-3-11-046984-4 | doi = 10.1515/9783110470734-007 | pmid = 29394020 | pages = 1–42 | chapter = Cisplatin and Oxaliplatin: Our Current Understanding of Their Actions }}
* {{cite book | vauthors = Riddell IA, Lippard SJ | veditors = Sigel A, Sigel H, Freisinger E, Sigel RK | title = Metallo-Drugs: Development and Action of Anticancer Agents | series = Metal Ions in Life Sciences | volume = 18 | date = 2018 | publisher = de Gruyter GmbH | location = Berlin | isbn = 978-3-11-046984-4 | doi = 10.1515/9783110470734-007 | pmid = 29394020 | pages = 1–42 | chapter = Cisplatin and Oxaliplatin: Our Current Understanding of Their Actions }}
{{refend}}
{{refend}}
Line 154: Line 154:
* {{cite web| url = https://druginfo.nlm.nih.gov/drugportal/name/cisplatin | publisher = U.S. National Library of Medicine| work = Drug Information Portal | title = Cisplatin }}
* {{cite web| url = https://druginfo.nlm.nih.gov/drugportal/name/cisplatin | publisher = U.S. National Library of Medicine| work = Drug Information Portal | title = Cisplatin }}
* [https://publications.iarc.fr/_publications/media/download/3339/e9c601280dccaa5a877bbc1ef1bd8e4a683ec189.pdf IARC Monograph: "Cisplatin"]
* [https://publications.iarc.fr/_publications/media/download/3339/e9c601280dccaa5a877bbc1ef1bd8e4a683ec189.pdf IARC Monograph: "Cisplatin"]
* Wikiversity page for the International Ototoxicity Management Group: https://en.wikiversity.org/wiki/International_Ototoxicity_Management_Group_(IOMG)


{{Chemotherapeutic agents}}
{{Chemotherapeutic agents}}

Latest revision as of 02:51, 25 November 2024

"Cisplatine" redirects here. For the Brazilian province that existed from 1821 to 1828, see Cisplatina. For the conflict in that province, see Cisplatine War.

Cisplatin
Clinical data
Trade namesPlatinol, others
Other namesCisplatinum, platamin, neoplatin, cismaplat, cis-diamminedichloroplatinum(II) (CDDP)
AHFS/Drugs.comMonograph
MedlinePlusa684036
License data
Pregnancy
category
Routes of
administration		Intravenous
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability100% (IV)
Protein binding> 95%
Elimination half-life30–100 hours
ExcretionRenal
Identifiers
CAS Number
PubChem CID
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
PDB ligand
CompTox Dashboard (EPA)
ECHA InfoCard100.036.106 Edit this at Wikidata
Chemical and physical data
Formula[Pt(NH3)2Cl2]
Molar mass300.05 g·mol−1
3D model (JSmol)
  • [NH3+][Pt+2](Cl)(Cl)[NH3+]
  • InChI=1S/2ClH.2H3N.Pt/h2*1H;2*1H3;/q;;;;+2/p-2 checkY
  • Key:LXZZYRPGZAFOLE-UHFFFAOYSA-L checkY
 ☒NcheckY (what is this?)  (verify)

Cisplatin is a chemical compound with formula cis-[Pt(NH3)2Cl2]. It is a coordination complex of platinum that is used as a chemotherapy medication used to treat a number of cancers.[3] These include testicular cancer, ovarian cancer, cervical cancer, bladder cancer, head and neck cancer, esophageal cancer, lung cancer, mesothelioma, brain tumors and neuroblastoma.[3] It is given by injection into a vein.[3]

Common side effects include bone marrow suppression, hearing problems including severe hearing loss, kidney damage, and vomiting.[3][4][5] Other serious side effects include numbness, trouble walking, allergic reactions, electrolyte problems, and heart disease.[3] Use during pregnancy can cause harm to the developing fetus.[1][3] Cisplatin is in the platinum-based antineoplastic family of medications.[3] It works in part by binding to DNA and inhibiting its replication.[3]

Cisplatin was first reported in 1845 and licensed for medical use in 1978 and 1979.[6][3] It is on the World Health Organization's List of Essential Medicines.[7][8]

Medical use

[edit]

Cisplatin is administered intravenously as short-term infusion in normal saline for treatment of solid and haematological malignancies. It is used to treat various types of cancers, including sarcomas, some carcinomas (e.g., small cell lung cancer, squamous cell carcinoma of the head and neck and ovarian cancer), lymphomas, bladder cancer, cervical cancer,[9] and germ cell tumors.

The introduction of cisplatin as a standard treatment for testicular cancer improved remission rates from 5-10% before 1974 to 75-85% by 1984.[10]

Side effects

[edit]

Cisplatin has a number of side effects that can limit its use:

  • Nephrotoxicity (kidney damage) is the primary dose-limiting side effect and is of major clinical concern. Cisplatin selectively accumulates into the proximal tubule via basolateral-to-apical transport, where it disrupts mitochondrial energetics and endoplasmic reticulum Ca2+ homeostasis and stimulates reactive oxygen species and pro-inflammatory cytokines.[11] Multiple mitigation strategies are being explored clinically and pre-clinically, including hydration regimens, amifostine, transporter inhibitors, antioxidants, anti-inflammatories, and epoxyeicosatrienoic acids and their analogues.[11][12]
  • 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.[13] 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. Cisplatin noncompetitively inhibits an archetypal, membrane-bound mechanosensitive sodium-hydrogen ion transporter known as NHE-1.[13] 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.[13] Cisplatin can increase levels of sphingosine-1-phosphate in the central nervous system, contributing to the development of post-chemotherapy cognitive impairment.[14][15]
  • 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 and hearing loss associated with cisplatin can be severe and is considered to be a dose-limiting side effect.[5] 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. In September 2022, the U.S. Food and Drug Administration (FDA) approved sodium thiosulfate under the brand name Pedmark to lessen the risk of ototoxicity and hearing loss in people receiving cisplatin.[16][17][18] There is ongoing investigation of acetylcysteine injections as a preventative measure.[5][19]
  • 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.[20]

Pharmacology

[edit]

Cisplatin interferes with DNA replication, which kills the fastest proliferating cells, which in theory are cancerous. Following administration, one chloride ion is slowly displaced by water to give the aquo complex cis-[PtCl(NH3)2(H2O)]+, in a process termed aquation. Dissociation of the chloride is favored inside the cell because the intracellular chloride concentration is only 3–20% of the approximately 100 mM chloride concentration in the extracellular fluid.[21][22]

The water molecule in cis-[PtCl(NH3)2(H2O)]+ is itself easily displaced by the N-heterocyclic bases on DNA. Guanine preferentially binds. A model compound has been prepared and crystals were examined by X-ray crystallography[23]

Subsequent to formation of [PtCl(guanine-DNA)(NH3)2]+, crosslinking can occur via displacement of the other chloride, typically by another guanine.[24] Cisplatin crosslinks DNA in several 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, apoptosis induced by cisplatin on human colon cancer cells was shown to depend on the mitochondrial serine-protease Omi/Htra2.[25] Since this was only demonstrated for colon carcinoma cells, it remains an open question whether the Omi/Htra2 protein participates in the cisplatin-induced apoptosis in carcinomas from other tissues.[25]

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. Coordination chemists have obtained crystals of the products of reacting cisplain with small models of DNA. Here is a POVray plot of the platinum binding to a small model of DNA.[26]

A POVray plot of the atomic coordinates for the cis Pt(NH3)2 and short fragment of DNA which was reported by Stephen J. Lippard in Science 1985

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.[27]

Cisplatin resistance

[edit]

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, increased DNA repair or changes in metabolism.[28][29] 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.[29] The drug paclitaxel may be useful in the treatment of cisplatin-resistant cancer; the mechanism for this activity is as yet unknown.[30]

Transplatin

[edit]

Transplatin, the trans-stereoisomer of cisplatin, has formula trans-[PtCl2(NH3)2] and does not exhibit a comparably useful pharmacological effect. Two mechanisms have been suggested to explain the reduced anticancer effect of transplatin. Firstly, the trans arrangement of the chloro ligands is thought to confer transplatin with greater chemical reactivity, causing transplatin to become deactivated before it reaches the DNA, where cisplatin exerts its pharmacological action. Secondly, the stereo-conformation of transplatin is such that it is unable to form the characteristic 1,2-intrastrand d(GpG) adducts formed by cisplatin in abundance.[31]

Molecular structure

[edit]

Cisplatin is the square planar coordination complex cis-[Pt(NH3)2Cl2].[32]: 286–8 [33]: 689  The prefix cis indicates the cis isomer in which two similar ligands are in adjacent positions.[32][33]: 550  The systematic chemical name of this molecule is cis–diamminedichloroplatinum,[32]: 286  where ammine with two m's indicates an ammonia (NH3) ligand, as opposed to an organic amine with one m.[32]: 284 

  • Solution structure of cisplatin (highlighted) interstrand GG adducts with double-stranded DNA. (PDB: 1DDP)
    Solution structure of cisplatin (highlighted) interstrand GG adducts with double-stranded DNA. (PDB: 1DDP)
  • 2.60Å resolution crystal structure of cisplatin (highlighted) intrastrand GG adducts with double-stranded DNA. Note: the hydrogens on amine ligands are not shown. (PDB: 1AIO)
    2.60Å resolution crystal structure of cisplatin (highlighted) intrastrand GG adducts with double-stranded DNA. Note: the hydrogens on amine ligands are not shown. (PDB: 1AIO)

History

[edit]

The compound cis-[Pt(NH3)2Cl2] was first described by Italian chemist Michele Peyrone in 1845, and known for a long time as Peyrone's salt.[34][35] The structure was deduced by Alfred Werner in 1893.[24] 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.[36] 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.[37][38] This finding led to the observation that cis-[PtCl2(NH3)2] was indeed highly effective at regressing the mass of sarcomas in rats.[39] 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.[24][40][41] and in the UK (and in several other European countries) in 1979.[42] Cisplatin was the first to be developed.[43] In 1983 pediatric oncologist Roger Packer began incorporating cisplatin into adjuvant chemotherapy for the treatment of childhood medulloblastoma.[44] The new protocol that he developed led to a marked increase in disease-free survival rates for patients with medulloblastoma, up to around 85%.[45] The Packer Protocol has since become a standard treatment for medulloblastoma. Likewise, cisplatin has been found to be particularly effective against testicular cancer, where its use improved the cure rate from 10% to 85%.[10]

Synthesis

[edit]

Syntheses of cisplatin start from potassium tetrachloroplatinate. Several procedures are available. One obstacle is the facile formation of Magnus's green salt (MGS), which has the same empirical formula as cisplatin. The traditional way to avoid MGS involves the conversion of K2PtCl4 to K2PtI4, as originally described by Dhara.[46][47] Reaction with ammonia forms PtI2(NH3)2 which is isolated as a yellow compound. When silver nitrate in water is added insoluble silver iodide precipitates and [Pt(OH2)2(NH3)2](NO3)2 remains in solution. Addition of potassium chloride will form the final product which precipitates[47] In the triiodo intermediate the addition of the second ammonia ligand is governed by the trans effect.[47]

A one-pot synthesis of cisplatin from K2PtCl4 has been developed. It relies on the slow release of ammonia from ammonium acetate.[48]

Research

[edit]

Cisplatin has been studied with Auger therapy to increase the therapeutic effects of cisplatin, without increasing normal tissue toxicities.[49] However, due to significant side effects, the search for structurally novel Pt(II) and Pd(II) compounds exhibiting antineoplastic activity is extremely important and aims to develop more effective and less toxic drugs.[50] Cisplatin-like molecules ([PtCl(NH3)2] and [Pt(NH3)Cl2]) linked by variable length alkandiamine chains have attracted some interest in cancer chemotherapy.[51][52][53]

References

[edit]
  1. ^ a b c d "Cisplatin Use During Pregnancy". Drugs.com. 12 September 2019. Retrieved 25 February 2020.
  2. ^ "FDA-sourced list of all drugs with black box warnings (Use Download Full Results and View Query links.)". nctr-crs.fda.gov. FDA. Retrieved 22 October 2023.
  3. ^ a b c d e f g h i "Cisplatin". The American Society of Health-System Pharmacists. Archived from the original on 21 December 2016. Retrieved 8 December 2016.
  4. ^ Oun R, Moussa YE, Wheate NJ (May 2018). "The side effects of platinum-based chemotherapy drugs: a review for chemists". Dalton Transactions. 47 (19): 6645–6653. doi:10.1039/c8dt00838h. PMID 29632935.
  5. ^ a b c Callejo A, Sedó-Cabezón L, Juan ID, Llorens J (July 2015). "Cisplatin-Induced Ototoxicity: Effects, Mechanisms and Protection Strategies". Toxics. 3 (3): 268–293. doi:10.3390/toxics3030268. PMC 5606684. PMID 29051464.
  6. ^ Fischer J, Ganellin CR (2006). Analogue-based Drug Discovery. John Wiley & Sons. p. 513. ISBN 9783527607495. Archived from the original on 20 December 2016.
  7. ^ World Health Organization (2019). World Health Organization model list of essential medicines: 21st list 2019. Geneva: World Health Organization. hdl:10665/325771. WHO/MVP/EMP/IAU/2019.06. License: CC BY-NC-SA 3.0 IGO.
  8. ^ World Health Organization (2021). World Health Organization model list of essential medicines: 22nd list (2021). Geneva: World Health Organization. hdl:10665/345533. WHO/MHP/HPS/EML/2021.02.
  9. ^ "Cisplatin". National Cancer Institute. 2 March 2007. Archived from the original on 8 October 2014. Retrieved 13 November 2014.
  10. ^ a b Einhorn LH (November 1990). "Treatment of testicular cancer: a new and improved model". Journal of Clinical Oncology. 8 (11): 1777–81. doi:10.1200/JCO.1990.8.11.1777. PMID 1700077.
  11. ^ a b Miller RP, Tadagavadi RK, Ramesh G, Reeves WB (October 2010). "Mechanisms of Cisplatin Nephrotoxicity". Toxins. 2 (11): 2490–2518. doi:10.3390/toxins2112490. PMC 3153174. PMID 22069563.
  12. ^ Singh N, Vik A, Lybrand DB, Morisseau C, Hammock BD (November 2021). "New Alkoxy- Analogues of Epoxyeicosatrienoic Acids Attenuate Cisplatin Nephrotoxicity In Vitro via Reduction of Mitochondrial Dysfunction, Oxidative Stress, Mitogen-Activated Protein Kinase Signaling, and Caspase Activation". Chemical Research in Toxicology. 34 (12): 2579–2591. doi:10.1021/acs.chemrestox.1c00347. PMC 8853703. PMID 34817988.
  13. ^ a b c Milosavljevic N, Duranton C, Djerbi N, Puech PH, Gounon P, Lagadic-Gossmann D, et al. (October 2010). "Nongenomic effects of cisplatin: acute inhibition of mechanosensitive transporters and channels without actin remodeling". Cancer Research. 70 (19): 7514–22. doi:10.1158/0008-5472.CAN-10-1253. PMID 20841472.
  14. ^ Squillace S, Niehoff ML, Doyle TM, Green M, Esposito E, Cuzzocrea S, Arnatt CK, Spiegel S, Farr SA, Salvemini D (September 2022). "Sphingosine-1-phosphate receptor 1 activation in the central nervous system drives cisplatin-induced cognitive impairment". The Journal of Clinical Investigation. 132 (17). doi:10.1172/JCI157738. PMC 9433103. PMID 36047496.
  15. ^ "Unlocking the Mystery of "Chemo Brain"". Neuroscience News. 2 September 2022.
  16. ^ Orgel E, Villaluna D, Krailo MD, Esbenshade A, Sung L, Freyer DR (May 2022). "Sodium thiosulfate for prevention of cisplatin-induced hearing loss: updated survival from ACCL0431". The Lancet. Oncology. 23 (5): 570–572. doi:10.1016/S1470-2045(22)00155-3. PMC 9635495. PMID 35489339.
  17. ^ Winstead E (6 October 2022). "Sodium Thiosulfate Reduces Hearing Loss in Kids with Cancer". National Cancer Institute. Retrieved 9 March 2023.
  18. ^ "FDA approves sodium thiosulfate to reduce the risk of ototoxicity associated with cisplatin in pediatric patients with localized, non-metastatic solid tumors". Food and Drug Administration. 20 September 2022. Retrieved 9 March 2023.
  19. ^ Sarafraz Z, Ahmadi A, Daneshi A (June 2018). "Transtympanic Injections of N-acetylcysteine and Dexamethasone for Prevention of Cisplatin-Induced Ototoxicity: Double Blind Randomized Clinical Trial". The International Tinnitus Journal. 22 (1): 40–45. doi:10.5935/0946-5448.20180007. PMID 29993216.
  20. ^ Levi JA, Aroney RS, Dalley DN (June 1981). "Haemolytic anaemia after cisplatin treatment". British Medical Journal. 282 (6281): 2003–4. doi:10.1136/bmj.282.6281.2003. PMC 1505958. PMID 6788166.
  21. ^ Wang D, Lippard SJ (April 2005). "Cellular processing of platinum anticancer drugs". Nature Reviews. Drug Discovery. 4 (4): 307–320. doi:10.1038/nrd1691. PMID 15789122. S2CID 31357727.
  22. ^ Johnstone TC, Suntharalingam K, Lippard SJ (March 2016). "The Next Generation of Platinum Drugs: Targeted Pt(II) Agents, Nanoparticle Delivery, and Pt(IV) Prodrugs". Chemical Reviews. 116 (5): 3436–3486. doi:10.1021/acs.chemrev.5b00597. PMC 4792284. PMID 26865551.
  23. ^ Orbell JD, Solorzano C, Marzilli LG, Kistenmacher TJ (October 1982). "Preparation and structure of cis-chlorodiammine (N2, N2-dimethyl-9-methylguanine) platinum (II) hexafluorophosphate. A model for the intermediate in the proposed crosslinking mode of action of platinum (II) antitumor agents". Inorganic Chemistry. 21 (10): 3806–3810. doi:10.1021/ic00140a041.
  24. ^ a b c Trzaska S (20 June 2005). "Cisplatin". Chemical & Engineering News. 83 (25): 52. doi:10.1021/cen-v083n025.p052.
  25. ^ a b 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". Journal of Chemotherapy. 20 (3): 348–354. doi:10.1179/joc.2008.20.3.348. PMID 18606591. S2CID 11052459.
  26. ^ Sherman SE, Gibson D, Wang AH, Lippard SJ (October 1985). "X-ray structure of the major adduct of the anticancer drug cisplatin with DNA: cis-[Pt(NH3)2(d(pGpG))]". Science. 230 (4724): 412–7. Bibcode:1985Sci...230..412S. doi:10.1126/science.4048939. PMID 4048939.
  27. ^ Hu J, Lieb JD, Sancar A, Adar S (October 2016). "Cisplatin DNA damage and repair maps of the human genome at single-nucleotide resolution". PNAS. 113 (41): 11507–11512. Bibcode:2016PNAS..11311507H. doi:10.1073/pnas.1614430113. PMC 5068337. PMID 27688757. S2CID 11052459.
  28. ^ Cruz-Bermúdez A, Laza-Briviesca R, Vicente-Blanco RJ, García-Grande A, Coronado MJ, Laine-Menéndez S, et al. (May 2019). "Cisplatin resistance involves a metabolic reprogramming through ROS and PGC-1α in NSCLC which can be overcome by OXPHOS inhibition". Free Radical Biology & Medicine. 135: 167–181. doi:10.1016/j.freeradbiomed.2019.03.009. hdl:10486/688357. PMID 30880247.
  29. ^ a b Stordal B, Davey M (November 2007). "Understanding cisplatin resistance using cellular models" (PDF). IUBMB Life. 59 (11): 696–699. doi:10.1080/15216540701636287. PMID 17885832. S2CID 30879019.
  30. ^ Stordal B, Pavlakis N, Davey R (December 2007). "A systematic review of platinum and taxane resistance from bench to clinic: an inverse relationship" (PDF). Cancer Treatment Reviews. 33 (8): 688–703. doi:10.1016/j.ctrv.2007.07.013. hdl:2123/4068. PMID 17881133.
  31. ^ Coluccia M, Natile G (January 2007). "Trans-platinum complexes in cancer therapy". Anti-Cancer Agents in Medicinal Chemistry. 7 (1): 111–123. doi:10.2174/187152007779314080. PMID 17266508.
  32. ^ a b c d Miessler GL, Tarr DA (1999). Inorganic Chemistry (2nd ed.). Prentice Hall. ISBN 978-0-13-841891-5.
  33. ^ a b Housecroft CE, Sharpe AG (2005). Inorganic Chemistry (2nd ed.). Pearson Prentice Hall. ISBN 978-0-130-39913-7.
  34. ^ Kauffman GB, Pentimalli R, Hall MD (2010). "Michele Peyrone (1813–1883), Discoverer of Cisplatin". Platinum Metals Review. 54 (4): 250–256. doi:10.1595/147106710X534326. Retrieved 3 October 2022. This biographical article aims to present, for the first time in the English language, a summary of his life and the achievements that he made during his scientific career.
  35. ^ Peyrone M (1844). "Ueber die Einwirkung des Ammoniaks auf Platinchlorür" [On the action of ammonia on platinum chloride]. Ann. Chem. Pharm. 51 (1): 1–29. doi:10.1002/jlac.18440510102.
  36. ^ Rosenberg B, Vancamp L, Krigas T (February 1965). "Inhibition of cell division in Escherichia coli by electrolysis products from a platinum electrode". Nature. 205 (4972): 698–9. Bibcode:1965Natur.205..698R. doi:10.1038/205698a0. PMID 14287410. S2CID 9543916.
  37. ^ 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". The Journal of Biological Chemistry. 242 (6): 1347–52. doi:10.1016/S0021-9258(18)96186-7. PMID 5337590.
  38. ^ Christie DA, Tansey EM (2007). Christie DA, Tansey EM, Thomson AJ (eds.). The Discovery, Use and Impact of Platinum Salts as Chemotherapy Agent for Cancer. Wellcome Trust Witnesses to Twentieth Century Medicine. Vol. 30. pp. 6–15. ISBN 978-0-85484-112-7.
  39. ^ Rosenberg B, VanCamp L, Trosko JE, Mansour VH (April 1969). "Platinum compounds: a new class of potent antitumour agents". Nature. 222 (5191): 385–6. Bibcode:1969Natur.222..385R. doi:10.1038/222385a0. PMID 5782119. S2CID 32398470.
  40. ^ Carpenter DP (2010). Reputation and power: organizational image and pharmaceutical regulation at the FDA. Princeton, NJ: Princeton University Press. ISBN 978-0-691-14180-0.
  41. ^ "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 15 July 2009.
  42. ^ Wiltshaw E (1979). "Cisplatin in the treatment of cancer". Platinum Metals Review. 23 (3): 90–8. doi:10.1595/003214079X2339098. S2CID 267470502.
  43. ^ Kelland L (2007). "The resurgence of platinum-based cancer chemotherapy". Nature Reviews Cancer. 7 (8): 573–584. doi:10.1038/nrc2167. PMID 17625587. S2CID 205468214.
  44. ^ Packer RJ, Sutton LN, Elterman R, Lange B, Goldwein J, Nicholson HS, et al. (November 1994). "Outcome for children with medulloblastoma treated with radiation and cisplatin, CCNU, and vincristine chemotherapy". Journal of Neurosurgery. 81 (5): 690–8. doi:10.3171/jns.1994.81.5.0690. PMID 7931615.
  45. ^ Packer RJ, Sutton LN, Goldwein JW, Perilongo G, Bunin G, Ryan J, et al. (March 1991). "Improved survival with the use of adjuvant chemotherapy in the treatment of medulloblastoma". Journal of Neurosurgery. 74 (3): 433–40. doi:10.3171/jns.1991.74.3.0433. PMID 1847194.
  46. ^ Dhara SC (1970). "Cisplatin". Indian J. Chem. 8: 123–134.
  47. ^ a b c Alderden RA, Hall MD, Hambley TW (2006). "The Discovery and Development of Cisplatin". J. Chem. Educ. 83 (5): 728. Bibcode:2006JChEd..83..728A. doi:10.1021/ed083p728. S2CID 29546931.
  48. ^ Kukushikin VY, Oskarsson Å, Elding LI, Farrell N (2007). "Facile Synthesis of Isomerically Pure cis -Dichlorodiammineplatinum(II), Cisplatin". Facile Synthesis of Isomerically Pure cis -Dichlorodiammineplatinum(II), Cisplatin. Inorganic Syntheses. Vol. 32. pp. 141–144. doi:10.1002/9780470132630.ch23. ISBN 9780470132630.
  49. ^ Ku A, Facca VJ, Cai Z, Reilly RM (October 2019). "Auger electrons for cancer therapy - a review". EJNMMI Radiopharmacy and Chemistry. 4 (1): 27. doi:10.1186/s41181-019-0075-2. PMC 6800417. PMID 31659527.
  50. ^ Fiuza SM, Amado AM, Oliveira PJ, Sardão VA, De Carvalho LB, Marques MP (2006). "Pt(II) vs Pd(II) Polyamine Complexes as New Anticancer Drugs: A Structure- Activity Study". Letters in Drug Design & Discovery. 3 (3): 149–151. doi:10.2174/157018006776286989. hdl:10316/45139.
  51. ^ Teixeira LJ, Seabra M, Reis E, da Cruz MT, de Lima MC, Pereira E, et al. (May 2004). "Cytotoxic activity of metal complexes of biogenic polyamines: polynuclear platinum(II) chelates". Journal of Medicinal Chemistry. 47 (11): 2917–2925. doi:10.1021/jm0311238. hdl:10316/10605. PMID 15139770.
  52. ^ Vinci D, Chateigner D (1 December 2022). "Synthesis and structural characterization of a new dinuclear platinum(III) complex, [Pt 2 Cl 4 (NH 3 ) 2 {μ-HN=C(O)Bu t } 2 ]". Acta Crystallographica Section B Structural Science, Crystal Engineering and Materials. 78 (6): 835–841. doi:10.1107/S2052520622009660. ISSN 2052-5206. PMC 9728019.
  53. ^ Omondi RO, Ojwach SO, Jaganyi D (November 2020). "Review of comparative studies of cytotoxic activities of Pt(II), Pd(II), Ru(II)/(III) and Au(III) complexes, their kinetics of ligand substitution reactions and DNA/BSA interactions". Inorganica Chimica Acta. 512: 119883. doi:10.1016/j.ica.2020.119883. S2CID 225575546.

Further reading

[edit]
[edit]
Retrieved from "https://en.wikipedia.org/enwiki/w/index.php?title=Cisplatin&oldid=1259428853"