Cisplatin | CAS#15663-27-1 | antineoplastic

MedKoo Cat#: 100160 | Name: Cisplatin

Description:

WARNING: This product is for research use only, not for human or veterinary use.

Cisplatin is an inorganic platinum agent (cis-diamminedichloroplatinum) with antineoplastic activity. Cisplatin forms highly reactive, charged, platinum complexes which bind to nucleophilic groups such as GC-rich sites in DNA, inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These cross-links result in apoptosis and cell growth inhibition.

Chemical Structure

Cisplatin

CAS#15663-27-1

Theoretical Analysis

MedKoo Cat#: 100160

Name: Cisplatin

CAS#: 15663-27-1

Chemical Formula: Cl2H6N2Pt

Exact Mass: 0.0000

Molecular Weight: 300.05

Elemental Analysis: Cl, 23.63; H, 2.02; N, 9.34; Pt, 65.02

Price and Availability

Size	Price	Availability
100mg	USD 90.00	Ready to ship
200mg	USD 150.00	Ready to ship
500mg	USD 250.00	Ready to ship
1g	USD 450.00	Ready to ship
2g	USD 750.00	Ready to ship
5g	USD 1,650.00	Ready to ship

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Related CAS #

No Data

Synonym

CACP; cisDDP; CDDP; cis-Diamminedichloroplatinum; Cisplatinum; NSC 119875; Cisplatin;

IUPAC/Chemical Name

(SP-4-2)-diamminedichloroplatinum; platinum, diaminedichloro-, cis-

InChi Key

LXZZYRPGZAFOLE-UHFFFAOYSA-L

InChi Code

InChI=1S/2ClH.2H3N.Pt/h2*1H;2*1H3;/q;;;;+2/p-2

SMILES Code

Cl[Pt-2]([NH3+])([NH3+])Cl

Appearance

Yellow solid powder

Purity

>98% (or refer to the Certificate of Analysis)

Shipping Condition

Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.

Storage Condition

Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).

Solubility

Soluble in DMF (5 mg/mL, need ultrasonic)

Shelf Life

>2 years if stored properly

Drug Formulation

This drug may be formulated in DMF

Stock Solution Storage

0 - 4 C for short term (days to weeks), or -20 C for long term (months).

HS Tariff Code

2843.90.0000

More Info

Product Data

Product Data

Certificate of Analysis

View CoA: current batch, Lot#A7T11K06

Safety Data Sheet (SDS)

View Safety Data Sheet (SDS)

Instruction

View handling instruction

Biological target:

Cisplatin (CDDP) is an antineoplastic chemotherapy agent by cross-linking with DNA and causing DNA damage in cancer cells.

In vitro activity:

Cisplatin primarily induces cell death by apoptosis and a defect in apoptotic signaling could also confer cisplatin resistance. There are two major pathways of apoptotic cell death The extrinsic pathway is initiated when ligands bind to the tumor necrosis factor-α (TNFα) receptor super family followed by oligomerization and recruitment of procaspase-8 via adaptor molecules to form the death-inducing signaling complex (DISC). The intrinsic pathway is initiated by cellular stress, such as DNA damage, resulting in release of cytochrome-c from the mitochondria causing activation of procaspase-9 through the interaction with apoptosis promoting activating factor-1 (APAF-1) and formation of an active apoptosome complex. Bcl-2 family proteins regulate DNA damage-induced apoptosis by regulating the release of mitochondrial cytochrome c in response to DNA damage. Cisplatin-induced genotoxic stress activates multiple signal transduction pathways, which can contribute to apoptosis or chemo resistance. Reference: Eur J Pharmacol. 2014 Oct 5; 740: 364–378. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146684/

In vivo activity:

Chk1 and Chk2 are checkpoint kinases that are activated by DNA damage signals mediated by ATM and ATR. Therefore, Chk1 and Chk2 phosphorylation were analyzed in long-term cisplatin-treated versus control mice with or without a final 12-h dose of cisplatin as another marker of whether cells were experiencing DNA damage. There was a clear difference in the dynamics of phosphorylation of these two DNA damage signaling proteins. Chk1 phosphorylation occurred in response to cisplatin in tumors from both naïve and long-term-treated mice (G1 vs. G2, and G3 vs. G4) (Supplemental Fig. S11), demonstrating that resistant tumors activate the DNA damage response, and, thus, that cisplatin is entering these cells. In contrast, Chk2 phosphorylation was induced after an initial dose of cisplatin (G1 vs. G2), and then remained high even in tumors that had not been given cisplatin for several weeks (G3 in Supplemental Fig. S11). This finding suggests that these two signaling pathways may be responding to distinct DNA damage signals as a result of cisplatin treatment—one that is transient (Chk1), and another that is persistent (Chk2). Furthermore, it suggests there is a fundamental difference in the DNA damage response mechanism in naïve and long-term cisplatin-treated lung tumors. Taken together, the data strongly argue that increased DNA damage repair is the predominant mechanism of cisplatin resistance in vivo in this model. Reference: Genes Dev. 2010 Apr 15; 24(8): 837–852. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854397/

	Solvent	mg/mL	mM
Solubility
	DMF	5.8	19.43
	PBS (pH 7.2)	1.0	3.33
	Water	1.4	4.58

Note: There can be variations in solubility for the same chemical from different vendors or different batches from the same vendor. The following factors can affect the solubility of the same chemical: solvent used for crystallization, residual solvent content, polymorphism, salt versus free form, degree of hydration, solvent temperature. Please use the solubility data as a reference only. Warming and sonication will facilitate dissolving. Still have questions? Please contact our Technical Support scientists.

Preparing Stock Solutions

The following data is based on the product molecular weight 300.05 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.

Concentration / Solvent Volume / Mass	1 mg	5 mg	10 mg
1 mM	1.15 mL	5.76 mL	11.51 mL
5 mM	0.23 mL	1.15 mL	2.3 mL
10 mM	0.12 mL	0.58 mL	1.15 mL
50 mM	0.02 mL	0.12 mL	0.23 mL

Formulation protocol:

1. Peltanova B, Liskova M, Gumulec J, Raudenska M, Polanska HH, Vaculovic T, Kalfert D, Grega M, Plzak J, Betka J, Masarik M. Sensitivity to Cisplatin in Head and Neck Cancer Cells Is Significantly Affected by Patient-Derived Cancer-Associated Fibroblasts. Int J Mol Sci. 2021 Feb 15;22(4):1912. doi: 10.3390/ijms22041912. PMID: 33671869; PMCID: PMC7918851. 2. Dasari S, Tchounwou PB. Cisplatin in cancer therapy: molecular mechanisms of action. Eur J Pharmacol. 2014 Oct 5;740:364-78. doi: 10.1016/j.ejphar.2014.07.025. Epub 2014 Jul 21. PMID: 25058905; PMCID: PMC4146684. 3. Oliver TG, Mercer KL, Sayles LC, Burke JR, Mendus D, Lovejoy KS, Cheng MH, Subramanian A, Mu D, Powers S, Crowley D, Bronson RT, Whittaker CA, Bhutkar A, Lippard SJ, Golub T, Thomale J, Jacks T, Sweet-Cordero EA. Chronic cisplatin treatment promotes enhanced damage repair and tumor progression in a mouse model of lung cancer. Genes Dev. 2010 Apr 15;24(8):837-52. doi: 10.1101/gad.1897010. PMID: 20395368; PMCID: PMC2854397. 4. Shin JN, Seo YW, Kim M, Park SY, Lee MJ, Lee BR, Oh JW, Seol DW, Kim TH. Cisplatin inactivation of caspases inhibits death ligand-induced cell death in vitro and fulminant liver damage in mice. J Biol Chem. 2005 Mar 18;280(11):10509-15. doi: 10.1074/jbc.M413865200. Epub 2005 Jan 5. PMID: 15634686.

In vitro protocol:

In vivo protocol:

1. Oliver TG, Mercer KL, Sayles LC, Burke JR, Mendus D, Lovejoy KS, Cheng MH, Subramanian A, Mu D, Powers S, Crowley D, Bronson RT, Whittaker CA, Bhutkar A, Lippard SJ, Golub T, Thomale J, Jacks T, Sweet-Cordero EA. Chronic cisplatin treatment promotes enhanced damage repair and tumor progression in a mouse model of lung cancer. Genes Dev. 2010 Apr 15;24(8):837-52. doi: 10.1101/gad.1897010. PMID: 20395368; PMCID: PMC2854397. 2. Shin JN, Seo YW, Kim M, Park SY, Lee MJ, Lee BR, Oh JW, Seol DW, Kim TH. Cisplatin inactivation of caspases inhibits death ligand-induced cell death in vitro and fulminant liver damage in mice. J Biol Chem. 2005 Mar 18;280(11):10509-15. doi: 10.1074/jbc.M413865200. Epub 2005 Jan 5. PMID: 15634686.

1: de Godoy Torso N, Pereira JKN, Visacri MB, Vasconcelos PENS, Loren P, Saavedra K, Saavedra N, Salazar LA, Moriel P. Dysregulated MicroRNAs as Biomarkers or Therapeutic Targets in Cisplatin-Induced Nephrotoxicity: A Systematic Review. Int J Mol Sci. 2021 Nov 25;22(23):12765. doi: 10.3390/ijms222312765. PMID: 34884570; PMCID: PMC8657822. 2: Hu X, Ma Z, Wen L, Li S, Dong Z. Autophagy in Cisplatin Nephrotoxicity during Cancer Therapy. Cancers (Basel). 2021 Nov 10;13(22):5618. doi: 10.3390/cancers13225618. PMID: 34830772; PMCID: PMC8616020. 3: Rahimi A, Asadi F, Rezghi M, Kazemi S, Soorani F, Memariani Z. Natural products against cisplatin-induced male reproductive toxicity: A comprehensive review. J Biochem Mol Toxicol. 2021 Nov 24:e22970. doi: 10.1002/jbt.22970. Epub ahead of print. PMID: 34820939. 4: Cheng Y, Li S, Gao L, Zhi K, Ren W. The Molecular Basis and Therapeutic Aspects of Cisplatin Resistance in Oral Squamous Cell Carcinoma. Front Oncol. 2021 Oct 22;11:761379. doi: 10.3389/fonc.2021.761379. PMID: 34746001; PMCID: PMC8569522. 5: Atashi F, Vahed N, Emamverdizadeh P, Fattahi S, Paya L. Drug resistance against 5-fluorouracil and cisplatin in the treatment of head and neck squamous cell carcinoma: A systematic review. J Dent Res Dent Clin Dent Prospects. 2021 Summer;15(3):219-225. doi: 10.34172/joddd.2021.036. Epub 2021 Aug 25. PMID: 34712414; PMCID: PMC8538146. 6: Abadi AJ, Mirzaei S, Mahabady MK, Hashemi F, Zabolian A, Hashemi F, Raee P, Aghamiri S, Ashrafizadeh M, Aref AR, Hamblin MR, Hushmandi K, Zarrabi A, Sethi G. Curcumin and its derivatives in cancer therapy: Potentiating antitumor activity of cisplatin and reducing side effects. Phytother Res. 2021 Oct 25. doi: 10.1002/ptr.7305. Epub ahead of print. PMID: 34697839. 7: Perše M. Cisplatin Mouse Models: Treatment, Toxicity and Translatability. Biomedicines. 2021 Oct 7;9(10):1406. doi: 10.3390/biomedicines9101406. PMID: 34680523; PMCID: PMC8533586. 8: Abd Rashid N, Abd Halim SAS, Teoh SL, Budin SB, Hussan F, Adib Ridzuan NR, Abdul Jalil NA. The role of natural antioxidants in cisplatin-induced hepatotoxicity. Biomed Pharmacother. 2021 Dec;144:112328. doi: 10.1016/j.biopha.2021.112328. Epub 2021 Oct 13. PMID: 34653753. 9: Berkel C, Cacan E. Estrogen- and estrogen receptor (ER)-mediated cisplatin chemoresistance in cancer. Life Sci. 2021 Dec 1;286:120029. doi: 10.1016/j.lfs.2021.120029. Epub 2021 Oct 8. PMID: 34634322. 10: Moghbeli M. MicroRNAs as the critical regulators of Cisplatin resistance in ovarian cancer cells. J Ovarian Res. 2021 Sep 30;14(1):127. doi: 10.1186/s13048-021-00882-1. PMID: 34593006; PMCID: PMC8485521. 11: Mapuskar KA, Steinbach EJ, Zaher A, Riley DP, Beardsley RA, Keene JL, Holmlund JT, Anderson CM, Zepeda-Orozco D, Buatti JM, Spitz DR, Allen BG. Mitochondrial Superoxide Dismutase in Cisplatin-Induced Kidney Injury. Antioxidants (Basel). 2021 Aug 24;10(9):1329. doi: 10.3390/antiox10091329. PMID: 34572961; PMCID: PMC8469643. 12: Mu Q, Lv Y, Luo C, Liu X, Huang C, Xiu Y, Tang L. Research Progress on the Functions and Mechanism of circRNA in Cisplatin Resistance in Tumors. Front Pharmacol. 2021 Sep 9;12:709324. doi: 10.3389/fphar.2021.709324. PMID: 34566636; PMCID: PMC8458655. 13: Corbeau A, Kuipers SC, de Boer SM, Horeweg N, Hoogeman MS, Godart J, Nout RA. Correlations between bone marrow radiation dose and hematologic toxicity in locally advanced cervical cancer patients receiving chemoradiation with cisplatin: a systematic review. Radiother Oncol. 2021 Nov;164:128-137. doi: 10.1016/j.radonc.2021.09.009. Epub 2021 Sep 21. PMID: 34560187. 14: Xu XF, Yang XK, Song Y, Chen BJ, Yu X, Xu T, Chen ZL. Dysregulation of Non- coding RNAs mediates Cisplatin Resistance in Hepatocellular Carcinoma and therapeutic strategies. Pharmacol Res. 2021 Sep 17:105906. doi: 10.1016/j.phrs.2021.105906. Epub ahead of print. PMID: 34543740. 15: Mu C, Wang XL, Ruan Y, Sun JJ, Hu XR, Cheng Y. Recent advances in the contribution of circRNAs to cisplatin chemotherapy resistance in cancers. Neoplasma. 2021 Nov;68(6):1119-1131. doi: 10.4149/neo_2021_210624N846. Epub 2021 Sep 16. PMID: 34533032. 16: Falco A, de Oliveira TB, Cacicedo J, Ospina AV, Ticona MÁ, Galindo H, Pereira MD, Aguilar-Ponce JL, Rueda-Domínguez A, Soria T, Taberna M, Iglesias L, Sowley T, Mesía R; TTCC group (Spanish Group for the Treatment of the Head and Neck Cancer). Ibero-American Expert Consensus on Squamous Cell Carcinoma of the Head and Neck Treatment in Patients Unable to Receive Cisplatin: Recommendations for Clinical Practice. Cancer Manag Res. 2021 Aug 26;13:6689-6703. doi: 10.2147/CMAR.S322411. PMID: 34471383; PMCID: PMC8405157. 17: Kryczka J, Kryczka J, Czarnecka-Chrebelska KH, Brzeziańska-Lasota E. Molecular Mechanisms of Chemoresistance Induced by Cisplatin in NSCLC Cancer Therapy. Int J Mol Sci. 2021 Aug 18;22(16):8885. doi: 10.3390/ijms22168885. PMID: 34445588; PMCID: PMC8396273. 18: Steyger PS. Mechanisms of Aminoglycoside- and Cisplatin-Induced Ototoxicity. Am J Audiol. 2021 Oct 11;30(3S):887-900. doi: 10.1044/2021_AJA-21-00006. Epub 2021 Aug 20. PMID: 34415784. 19: Prayuenyong P, Baguley DM, Kros CJ, Steyger PS. Preferential Cochleotoxicity of Cisplatin. Front Neurosci. 2021 Jul 26;15:695268. doi: 10.3389/fnins.2021.695268. PMID: 34381329; PMCID: PMC8350121. 20: Kiss RC, Xia F, Acklin S. Targeting DNA Damage Response and Repair to Enhance Therapeutic Index in Cisplatin-Based Cancer Treatment. Int J Mol Sci. 2021 Jul 30;22(15):8199. doi: 10.3390/ijms22158199. PMID: 34360968; PMCID: PMC8347825.

Pattarawat P, Hunt JT, Poloway J, Archibald CJ, Wang HR. A triple combination gemcitabine + romidepsin + cisplatin to effectively control triple-negative breast cancer tumor development, recurrence, and metastasis. Cancer Chemother Pharmacol. 2021 May 27. doi: 10.1007/s00280-021-04298-y. Epub ahead of print. PMID: 34043046.