Home>>Signaling Pathways>> DNA Damage/DNA Repair>> DNA/RNA Synthesis>>Oxaliplatin


Catalog No.: GC17716

Oxaliplatin is a cytotoxic chemotherapy drug used to treat cancer.

Oxaliplatin Chemical Structure

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Cell experiment [1]:

Cell lines

OSCC cells

Preparation Method

In order to determine the effect of oxaliplatin on cell viability, CAL27 cells and SCC25 cells were treated with different concentrations of oxaliplatin for 12, 24, and 48 hours.

Reaction Conditions

0-300uM Oxaliplatin for 12, 24, and 48 hours


Oxaliplatin inhibited cell viability, migration, and cloning formation of OSCC cells and induced cell death in vitro.

Animal experiment [2]:

Animal models

BALB/c mice

Preparation Method

Subjects were injected intraperitoneally (once every two days) with oxaliplatin (5 mg/kg in PBS, oxaliplatin group) or same volume of PBS (control group). After 21 days, mice were euthanized, and their xenografts were harvested and weighed.

Dosage form

5 mg/kg oxaliplatin for 21 days


Oxaliplatin inhibited tumor growth of OSCC and caused upregulation of PARP1 in vivo.


[1]. Li D, Kou Y, et,al. Oxaliplatin induces the PARP1-mediated parthanatos in oral squamous cell carcinoma by increasing production of ROS. Aging (Albany NY). 2021 Jan 20;13(3):4242-4257. doi: 10.18632/aging.202386. Epub 2021 Jan 20. PMID: 33495407; PMCID: PMC7906208.


Oxaliplatin is a cytotoxic chemotherapy drug used to treat cancer. Oxaliplatin works by interfering with the development of DNA in a cell. This helps to treat cancer which is caused by cells rapidly growing and dividing out of control.

Oxaliplatin can induce DNA damage in cancer cells. Besides,oxaliplatin can interfere with the cell cycle, promote apoptosis, and induce autophagy in tumor cells[2,3]. Oxaliplatin inhibited cell viability, migration, and cloning formation of OSCC cells and induced cell death in vitro[1]. Oxaliplatin inhibited the growth of HCCLM3 and Hep3B cells.Downregulation of the anti-apoptotic proteins Bcl-2 and Bcl-xL and upregulation of the pro-apoptotic protein Bax during oxaliplatin-induced apoptosis[6]. Oxaliplatin was found to be active against C32 and G361 cell lines with IC50 values of 49.48 and 9.07 uM (1 h exposure), 9.47 and 1.30 uM (4 h exposure), and 0.98 and 0.14 uM (24 h exposure), respectively. At a 24 h exposure oxaliplatin appears to be significantly more active than cisplatin against the G361 cell line[4]. 85-88% of all platinum from oxaliplatin was bound to plasma proteins within the first 5 h with an average half-life of 1.71 +/- 0.06 h. When oxaliplatin was incubated in whole blood, the erythrocytes took up 37.1 +/- 2.1% of the total platinum in 2 h (maximum uptake) which was not exchangeable into plasma[5].

The in vivo anticancer effect of oxaliplatin was studied using a nude mouse subcutaneously implanted with CAL27 cells. The average volume of tumors was markedly smaller in the oxaliplatin group than in the control group. Therefore, these results indicated that oxaliplatin inhibited the growth of xenograft OSCC cells in vivo, which was accompanied by the upregulated expression of PARP1[1]. Oxaliplatin-treated mice displayed reduced weight gain, mechanical allodynia, and exploratory behavior deficits that were not significantly improved by exercise[7]. When investigated oxaliplatin-induced haematological toxicities and splenomegaly in mice, Blood analysis showed dose dependent decreases in white and red blood cell counts, and significant changes in haematological indices.Spleen weight was significantly increased indicating splenomegaly, and red pulp tissue exhibited substantial dysplasia[8]. Oxaliplatin-treated mice displayed reduced weight gain and behavioral deficits. Mice treated over a shorter course had significantly increased STAT3 phosphorylation in gastrocnemius muscles. Mice receiving extended oxaliplatin treatment demonstrated reduced hindlimb muscle mass with upregulation of myopathy-associated genes Foxo3, MAFbx, and Bnip3[9].

[1]. Li D, Kou Y, et,al. Oxaliplatin induces the PARP1-mediated parthanatos in oral squamous cell carcinoma by increasing production of ROS. Aging (Albany NY). 2021 Jan 20;13(3):4242-4257. doi: 10.18632/aging.202386. Epub 2021 Jan 20. PMID: 33495407; PMCID: PMC7906208.
[2]. Wang X, Li M, et,al. On-Demand Autophagy Cascade Amplification Nanoparticles Precisely Enhanced Oxaliplatin-Induced Cancer Immunotherapy. Adv Mater. 2020 Aug;32(32):e2002160. doi: 10.1002/adma.202002160. Epub 2020 Jun 28. PMID: 32596861.
[3]. Yan S, Zhou N, et,al. PFKFB3 Inhibition Attenuates Oxaliplatin-Induced Autophagy and Enhances Its Cytotoxicity in Colon Cancer Cells. Int J Mol Sci. 2019 Oct 30;20(21):5415. doi: 10.3390/ijms20215415. PMID: 31671668; PMCID: PMC6862230.
[4]. Mohammed MQ, Retsas S. Oxaliplatin is active in vitro against human melanoma cell lines: comparison with cisplatin and carboplatin. Anticancer Drugs. 2000 Nov;11(10):859-63. doi: 10.1097/00001813-200011000-00010. PMID: 11142694.
[5]. Pendyala L, Creaven PJ. In vitro cytotoxicity, protein binding, red blood cell partitioning, and biotransformation of oxaliplatin. Cancer Res. 1993 Dec 15;53(24):5970-6. PMID: 8261411.
[6]. Wang Z, Zhou J, et,al. Oxaliplatin induces apoptosis in hepatocellular carcinoma cells and inhibits tumor growth. Expert Opin Investig Drugs. 2009 Nov;18(11):1595-604. doi: 10.1517/13543780903292626. PMID: 19780708.
[7]. Lees JG, Abdulla M, et,al. Effect of exercise on neuromuscular toxicity in oxaliplatin-treated mice. Muscle Nerve. 2021 Aug;64(2):225-234. doi: 10.1002/mus.27329. Epub 2021 Jun 12. PMID: 34036599.
[8]. Lees JG, White D, et,al. Oxaliplatin-induced haematological toxicity and splenomegaly in mice. PLoS One. 2020 Sep 2;15(9):e0238164. doi: 10.1371/journal.pone.0238164. PMID: 32877416; PMCID: PMC7467301.
[9]. Feather CE, Lees JG, et,al. Oxaliplatin induces muscle loss and muscle-specific molecular changes in Mice. Muscle Nerve. 2018 Apr;57(4):650-658. doi: 10.1002/mus.25966. Epub 2017 Oct 6. PMID: 28881481.

Chemical Properties

Cas No. 61825-94-3 SDF
Chemical Name (1R,2R)-cyclohexane-1,2-diamine;oxalate;platinum(2+)
Canonical SMILES C1CCC(C(C1)N)N.C(=O)(C(=O)[O-])[O-].[Pt+2]
Formula C8H14N2O4Pt M.Wt 397.29
Solubility ≥ 3.94mg/mL in Water with gentle warming Storage 4°C, protect from light
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

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Research Update

Oxaliplatin: Detection and Management of Hypersensitivity Reactions

Background: Oxaliplatin is used extensively for the treatment of gastrointestinal cancer and other malignancies, with increased frequency of use in recent years. Hypersensitivity reactions (HSRs) can pose a major problem in clinical practice because they can limit the use of oxaliplatin in the care of malignancies in which it has proven efficacy. Nurses play an integral role in the administration of oxaliplatin; therefore, they need to be well educated in the prevention, detection, and management of HSRs. Objectives: This article reviews the symptoms of HSRs associated with oxaliplatin, the specific management of HSRs associated with oxaliplatin, the role of desensitization, and the potential use of skin testing to better identify patients at risk for HSR. Methods: This article reviews the literature related to the diagnosis, prevention, and management of HSRs associated with oxaliplatin and outlines nurses' role. Findings: Oxaliplatin HSRs can occur at any cycle, but patients are at highest risk after they have received six prior infusions of oxaliplatin.

Oxaliplatin-induced peripheral neuropathy: clinical features, mechanisms, prevention and treatment

Oxaliplatin (OXA) is a commonly used platinum-based chemotherapy drug for colorectal cancer. OXA-induced peripheral neurotoxcity (OIPN) is a comprehensive adverse reaction of OXA. OIPN can be divided into acute and chronic types according to clinical features and different mechanisms. The main clinical features of acute OIPN are cold-sensitive sensory symptoms and neuropathic pain in limbs. In addition to the above symptoms, chronic OIPN also produces autonomic nerve dysfunction. The most important mechanism involved in acute OIPN is the alteration of voltage-gated Na + channels, and nuclear DNA damage in chronic OIPN. There are some methods like reducing exposure to cold, calcium and magnesium salts, amifostine could be beneficial in acute OIPN prevention and dose modification, changing in schedule glutathione, duloxetine, selective serotonin reuptake inhibitors, carbonic anhydrase inhibitor in chronic OIPN prevention. Recent updates are provided in this article in relation to the clinical features, potential mechanisms, prevention and treatment of OIPN.

Chemotherapy-induced peripheral neuropathy-part 2: focus on the prevention of oxaliplatin-induced neurotoxicity

Background: Chemotherapy-induced peripheral neuropathy (CIPN) is regarded as one of the most common dose-limiting adverse effects of several chemotherapeutic agents, such as platinum derivatives (oxaliplatin and cisplatin), taxanes, vinca alkaloids and bortezomib. CIPN affects more than 60% of patients receiving anticancer therapy and although it is a nonfatal condition, it significantly worsens patients' quality of life. The number of analgesic drugs used to relieve pain symptoms in CIPN is very limited and their efficacy in CIPN is significantly lower than that observed in other neuropathic pain types. Importantly, there are currently no recommended options for effective prevention of CIPN, and strong evidence for the utility and clinical efficacy of some previously tested preventive therapies is still limited.
Methods: The present article is the second one in the two-part series of review articles focused on CIPN. It summarizes the most recent advances in the field of studies on CIPN caused by oxaliplatin, the third-generation platinum-based antitumor drug used to treat colorectal cancer. Pharmacological properties of oxaliplatin, genetic, molecular and clinical features of oxaliplatin-induced neuropathy are discussed.
Results: Available therapies, as well as results from clinical trials assessing drug candidates for the prevention of oxaliplatin-induced neuropathy are summarized.
Conclusion: Emerging novel chemical structures-potential future preventative pharmacotherapies for CIPN caused by oxaliplatin are reported.

Lnc-RP11-536 K7.3/SOX2/HIF-1α signaling axis regulates oxaliplatin resistance in patient-derived colorectal cancer organoids

Background: Resistance to oxaliplatin is a major obstacle for the management of locally advanced and metastatic colon cancer (CC). Although long noncoding RNAs (lncRNAs) play key roles in CC, the relationships between lncRNAs and resistance to oxaliplatin have been poorly understood yet.
Methods: Chemo-sensitive and chemo-resistant organoids were established from colon cancer tissues of the oxaliplatin-sensitive or -resistant patients. Analysis of the patient cohort indicated that lnc-RP11-536 K7.3 had a potential oncogenic role in CC. Further, a series of functional in vitro and in vivo experiments were conducted to assess the effects of lnc-RP11-536 K7.3 on CC proliferation, glycolysis, and angiogenesis. RNA pull-down assay, luciferase reporter and fluorescent in situ hybridization assays were used to confirm the interactions between lnc-RP11-536 K7.3, SOX2 and their downstream target HIF-1α.
Results: In this study, we identified a novel lncRNA, lnc-RP11-536 K7.3, was associated with resistance to oxaliplatin and predicted a poor survival. Knockout of lnc-RP11-536 K7.3 inhibited the proliferation, glycolysis, and angiogenesis, whereas enhanced chemosensitivity in chemo-resistant organoids and CC cells both in vitro and in vivo. Furthermore, we found that lnc-RP11-536 K7.3 recruited SOX2 to transcriptionally activate USP7 mRNA expression. The accumulative USP7 resulted in deubiquitylation and stabilization of HIF-1α, thereby facilitating resistance to oxaliplatin.
Conclusion: In conclusion, our findings indicated that lnc-RP11-536 K7.3 could promote proliferation, glycolysis, angiogenesis, and chemo-resistance in CC by SOX2/USP7/HIF-1α signaling axis. This revealed a new insight into how lncRNA could regulate chemosensitivity and provide a potential therapeutic target for reversing resistance to oxaliplatin in the management of CC.

Camrelizumab plus gemcitabine and oxaliplatin (GEMOX) in patients with advanced biliary tract cancer: a single-arm, open-label, phase II trial

Background: Immune checkpoint inhibitors monotherapy has been studied in patients with advanced biliary tract cancer (BTC). The aim of this study was to assess the efficacy and safety of camrelizumab, plus gemcitabine and oxaliplatin (GEMOX) as first-line treatment in advanced BTC and explored the potential biomarkers associated with response.
Methods: In this single-arm, open-label, phase II study, we enrolled stage IV BTC patients. Participants received camrelizumab (3 mg/kg) plus gemcitabine (800 mg/m2) and oxaliplatin (85 mg/m2). Primary endpoints were 6-month progression-free survival (PFS) rate and safety. Secondary endpoints were objective response rate (ORR), PFS and overall survival (OS). Exploratory endpoints included association between response and tumor mutational burden (TMB), blood TMB, dynamic change of ctDNA and immune microenvironment.
Results: 54 patients with advanced BTC were screened, of whom 38 eligible patients were enrolled. One patient withdrew informed consent before first dose treatment. Median follow-up was 11.8 months. The 6-month PFS rate was 50% (95% CI 33 to 65). Twenty (54%) out of 37 patients had an objective response. The median PFS was 6.1 months and median OS was 11.8 months. The most common treatment-related adverse events (TRAEs) were fatigue (27 (73%)) and fever (27 (73%)). The most frequent grade 3 or worse TRAEs were hypokalemia (7 (19%)) and fatigue (6 (16%)). The ORR was 80% in patients with programmed cell death ligand-1 (PD-L1) tumor proportion score (TPS) ≥1% versus 53.8% in PD-L1 TPS <1%. There was no association between response and TMB, blood TMB, immune proportion score or immune cells (p>0.05), except that PFS was associated with blood TMB. Patients with positive post-treatment ctDNA had shorter PFS (p=0.007; HR, 2.83; 95% CI 1.27 to 6.28).
Conclusion: Camrelizumab plus GEMOX showed a promising antitumor activity and acceptable safety profile as first-line treatment in advanced BTC patients. Potential biomarkers are needed to identify patients who might respond to camrelizumab plus GEMOX.
Trial registration number: NCT03486678.


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