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Eflornithine (DFMO)

Catalog No.GC30283

Eflornithine (DFMO) is a specific, irreversible inhibitor of the enzyme ornithine decarboxylase.

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Eflornithine (DFMO) Chemical Structure

Cas No.:70052-12-9

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Sample solution is provided at 25 µL, 10mM.

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Cell experiment [1]:

Cell lines

OVCAR5 and SKOV3 cells

Preparation Method

Cells were treated with 0.5 mM Eflornithine (DFMO) and rucaparib.

Reaction Conditions

0.5 mM Eflornithine ;72h


Eflornithine Sensitizes homologous recombination (HR)-Competent Ovarian Cancer Cells to Rucaparib.

Animal experiment [2]:

Animal models

Pancreas of athymic (nu/nu) mice (Human pancreatic L3.6pl tumor model)

Preparation Method

Mice were treated for two weeks with control, GW5074 (1 mg/kg), Eflornithine (1% w/v) and Eflornithine + GW5074 after a week post orthotopic tumor cell implantation.

Dosage form

1% w/v Eflornithine in the drinking water; 48-72 h


Eflornithinealone markedly increases survival of pancreatic tumor-bearing mice in contrast with GW5074 across multiple dosing and tumor seeding strategies.


[1]. El Naggar O, Doyle B, et,al. Difluoromethylornithine (DFMO) Enhances the Cytotoxicity of PARP Inhibition in Ovarian Cancer Cells. Med Sci (Basel). 2022 May 26;10(2):28. doi: 10.3390/medsci10020028. PMID: 35736348; PMCID: PMC9230675.
[2].Nakkina SP, Gitto SB, et,al. DFMO Improves Survival and Increases Immune Cell Infiltration in Association with MYC Downregulation in the Pancreatic Tumor Microenvironment. Int J Mol Sci. 2021 Dec 7;22(24):13175. doi: 10.3390/ijms222413175. PMID: 34947972; PMCID: PMC8706739.


Eflornithine(DFMO) inhibits polyamine biosynthesis by irreversible inhibition of ornithine decarboxylase(ODC). It is a chemotherapeutic protectant that blocks angiogenesis. Its biological half-life is 8 hours[1-2].

Eflornithine (0.5 mM DFMO;72h) sensitizes homologous recombination (HR)-Competent Ovarian Cancer Cells to Rucaparib [3]. Combination of Eflornithine (1 mM; 48 h) and Thymoquinone (TQ) significantly reduced cell viability and resulted in significant synergistic effects on apoptosis when compared to either Eflornithine or TQ alone in Jurkat cells [4]. Eflornithine (5 mM;72h) treatment leads to the accumulation of the cyclin-dependent kinase inhibitor p27(Kip1) protein and causes p27(Kip1)/Rb-coupled G (1) cell cycle arrest in MYCN-amplified NB tumor cells through a process that involves p27(Kip1) phosphorylation at residues Ser10 and Thr198[5].

Eflornithine (1% w/v in the drinking water; 48-72 h) alone markedly increases survival of pancreatic tumor-bearing mice in contrast with GW5074 across multiple dosing and tumor seeding strategies [6]. The Kras(G12D/+) mice fed Eflornithine at 0.1% and 0.2% in the diet showed a significant inhibition of pancreatic ductal adenocarcinoma (PDAC) incidence compared with mice fed control diet [7].

[1]. Drugs and Lactation Database (LactMed®) [Internet]. Bethesda (MD): National Institute of Child Health and Human Development; 2006-. Eflornithine. 2021 Dec 20. PMID: 29999676.
[2]. Kang CN, Shah M, et,al. Hair Removal Practices: A Literature Review. Skin Therapy Lett. 2021 Sep;26(5):6-11. PMID: 34524781.
[3]. El Naggar O, Doyle B, et,al. Difluoromethylornithine (DFMO) Enhances the Cytotoxicity of PARP Inhibition in Ovarian Cancer Cells. Med Sci (Basel). 2022 May 26;10(2):28. doi: 10.3390/medsci10020028. PMID: 35736348; PMCID: PMC9230675.
[4]. Alhosin M, Razvi SSI, et,al. Thymoquinone and Difluoromethylornithine (DFMO) Synergistically Induce Apoptosis of Human Acute T Lymphoblastic Leukemia Jurkat Cells Through the Modulation of Epigenetic Pathways. Technol Cancer Res Treat. 2020 Jan-Dec;19:1533033820947489. doi: 10.1177/1533033820947489. PMID: 32912061; PMCID: PMC7488875.
[5]. Koomoa DL, Geerts D, et,al. DFMO/eflornithine inhibits migration and invasion downstream of MYCN and involves p27Kip1 activity in neuroblastoma. Int J Oncol. 2013 Apr;42(4):1219-28. doi: 10.3892/ijo.2013.1835. Epub 2013 Feb 21. PMID: 23440295; PMCID: PMC3622674.
[6]. Nakkina SP, Gitto SB, et,al. DFMO Improves Survival and Increases Immune Cell Infiltration in Association with MYC Downregulation in the Pancreatic Tumor Microenvironment. Int J Mol Sci. 2021 Dec 7;22(24):13175. doi: 10.3390/ijms222413175. PMID: 34947972; PMCID: PMC8706739.
[7]. Mohammed A, Janakiram NB, et,al. Eflornithine (DFMO) prevents progression of pancreatic cancer by modulating ornithine decarboxylase signaling. Cancer Prev Res (Phila). 2014 Dec;7(12):1198-209. doi: 10.1158/1940-6207.CAPR-14-0176. Epub 2014 Sep 23. PMID: 25248858; PMCID: PMC4310684.

Chemical Properties

Cas No. 70052-12-9 SDF
Canonical SMILES NC(CCCN)(C(F)F)C(O)=O
Formula C6H12F2N2O2 M.Wt 182.17
Solubility Soluble in H2O Storage Store at -20°C
General tips Please select the appropriate solvent to prepare the stock solution according to the solubility of the product in different solvents; once the solution is prepared, please store it in separate packages to avoid product failure caused by repeated freezing and thawing.Storage method and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored at -20°C, please use it within 1 month.
To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time.
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Research Update

DFMO Carbon Dots for Treatment of Neuroblastoma and Bioimaging

Neuroblastoma (NB) is a pediatric malignancy affecting the peripheral nervous system. Despite recent advancements in treatment, many children affected with NB continue to submit to this illness, and new therapeutic strategies are desperately needed. In recent years, studies of carbon dots (CDs) as nanocarriers have mostly focused on the delivery of anticancer agents because of their biocompatibility, good aqueous dissolution, and photostability. Their fluorescence properties, surface functionalities, and surface charges differ on the basis of the type of precursors used and the synthetic approach implemented. At present, most CDs are used as nanocarriers by directly linking them either covalently or electrostatically to drug molecules. Though most modern CDs are synthesized from large carbon macromolecules and conjugated to anticancerous drugs, constructing CDs from the anticancerous drugs and precursors themselves to increase antitumoral activity requires further investigation. Herein, CDs were synthesized using difluoromethylornithine (DFMO), an irreversible ornithine decarboxylase inhibitor commonly used in high-risk neuroblastoma treatment regiments. In this study, NB cell lines, SMS-KCNR and SK-N-AS, were treated with DFMO, the newly synthesized DFMO CDs, and conventional DFMO conjugated to black carbon dots. Bioimaging was done to determine the cellular localization of a fluorescent drug over time. The mobility of DNA mixed with DFMO CDs was evaluated by gel electrophoresis. DFMO CDs were effectively synthesized from DFMO precursor and characterized using spectroscopic methods. The DFMO CDs effectively reduced cell viability with increasing dose. The effects were dramatic in the N-MYC-amplified line SMS-KCNR at 500 米M, which is comparable to high doses of conventional DFMO at a 60-fold lower concentration. In vitro bioimaging as well as DNA electrophoresis showed that synthesized DFMO CDs were able to enter the nucleus of neuroblastoma cells and neuronal cells and interact with DNA. Our new DFMO CDs exhibit a robust advantage over conventional DFMO because they induce comparable reductions in viability at a dramatically lower concentration.

Difluoromethylornithine (DFMO) and AMXT 1501 inhibit capsule biosynthesis in pneumococci

Polyamines are small cationic molecules that have been linked to various cellular processes including replication, translation, stress response and recently, capsule regulation in Streptococcus pneumoniae (Spn, pneumococcus). Pneumococcal-associated diseases such as pneumonia, meningitis, and sepsis are some of the leading causes of death worldwide and capsule remains the principal virulence factor of this versatile pathogen. 汐-Difluoromethyl-ornithine (DFMO) is an irreversible inhibitor of the polyamine biosynthesis pathway catalyzed by ornithine decarboxylase and has a long history in modulating cell growth, polyamine levels, and disease outcomes in eukaryotic systems. Recent evidence shows that DFMO can also target arginine decarboxylation. Interestingly, DFMO-treated cells often escape polyamine depletion via increased polyamine uptake from extracellular sources. Here, we examined the potential capsule-crippling ability of DFMO and the possible synergistic effects of the polyamine transport inhibitor, AMXT 1501, on pneumococci. We characterized the changes in pneumococcal metabolites in response to DFMO and AMXT 1501, and also measured the impact of DFMO on amino acid decarboxylase activities. Our findings show that DFMO inhibited pneumococcal polyamine and capsule biosynthesis as well as decarboxylase activities, albeit, at a high concentration. AMXT 1501 at physiologically relevant concentration could inhibit both polyamine and capsule biosynthesis, however, in a serotype-dependent manner. In summary, this study demonstrates the utility of targeting polyamine biosynthesis and transport for pneumococcal capsule inhibition. Since targeting capsule biosynthesis is a promising way for the eradication of the diverse and pathogenic pneumococcal strains, future work will identify small molecules similar to DFMO/AMXT 1501, which act in a serotype-independent manner.

Probenecid increases renal retention and antitumor activity of DFMO in neuroblastoma

Background: Neuroblastoma (NB) is the most common extracranial solid tumor in children. Interference with the polyamine biosynthesis pathway by inhibition of MYCN-activated ornithine decarboxylase (ODC) is a validated approach. The ODC inhibitor 汐-difluoromethylornithine (DFMO, or Eflornithine) has been FDA-approved for the treatment of trypanosomiasis and hirsutism and has advanced to clinical cancer trials including NB as well as cancer-unrelated human diseases. One key challenge of DFMO is its rapid renal clearance and the need for high and frequent drug dosing during treatment.
Methods: We performed in vivo pharmacokinetic (PK), antitumorigenic, and molecular studies with DFMO/probenecid using NB patient-derived xenografts (PDX) in mice. We used LC-MS/MS, HPLC, and immunoblotting to analyze blood, brain tissue, and PDX tumor tissue samples collected from mice.
Results: The organic anion transport 1/3 (OAT 1/3) inhibitor probenecid reduces the renal clearance of DFMO and significantly increases the antitumor activity of DFMO in PDX of NB (P < 0.02). Excised tumors revealed that DFMO/probenecid treatment decreases polyamines putrescine and spermidine, reduces MYCN protein levels and dephosphorylates retinoblastoma (Rb) protein (p-RbSer795), suggesting DFMO/probenecid-induced cell cycle arrest.
Conclusion: Addition of probenecid as an adjuvant to DFMO therapy may be suitable to decrease overall dose and improve drug efficacy in vivo.

Dual targeting of polyamine synthesis and uptake in diffuse intrinsic pontine gliomas

Diffuse intrinsic pontine glioma (DIPG) is an incurable malignant childhood brain tumor, with no active systemic therapies and a 5-year survival of less than 1%. Polyamines are small organic polycations that are essential for DNA replication, translation and cell proliferation. Ornithine decarboxylase 1 (ODC1), the rate-limiting enzyme in polyamine synthesis, is irreversibly inhibited by difluoromethylornithine (DFMO). Herein we show that polyamine synthesis is upregulated in DIPG, leading to sensitivity to DFMO. DIPG cells compensate for ODC1 inhibition by upregulation of the polyamine transporter SLC3A2. Treatment with the polyamine transporter inhibitor AMXT 1501 reduces uptake of polyamines in DIPG cells, and co-administration of AMXT 1501 and DFMO leads to potent in vitro activity, and significant extension of survival in three aggressive DIPG orthotopic animal models. Collectively, these results demonstrate the potential of dual targeting of polyamine synthesis and uptake as a therapeutic strategy for incurable DIPG.

Difluoromethylornithine (DFMO) Enhances the Cytotoxicity of PARP Inhibition in Ovarian Cancer Cells

Ovarian cancer accounts for 3% of the total cancers in women, yet it is the fifth leading cause of cancer deaths among women. The BRCA1/2 germline and somatic mutations confer a deficiency of the homologous recombination (HR) repair pathway. Inhibitors of poly (ADP-ribose) polymerase (PARP), another important component of DNA damage repair, are somewhat effective in BRCA1/2 mutant tumors. However, ovarian cancers often reacquire functional BRCA and develop resistance to PARP inhibitors. Polyamines have been reported to facilitate the DNA damage repair functions of PARP. Given the elevated levels of polyamines in tumors, we hypothesized that treatment with the polyamine synthesis inhibitor, 汐-difluoromethylornithine (DFMO), may enhance ovarian tumor sensitivity to the PARP inhibitor, rucaparib. In HR-competent ovarian cancer cell lines with varying sensitivities to rucaparib, we show that co-treatment with DFMO increases the sensitivity of ovarian cancer cells to rucaparib. Immunofluorescence assays demonstrated that, in the presence of hydrogen peroxide-induced DNA damage, DFMO strongly inhibits PARylation, increases DNA damage accumulation, and reduces cell viability in both HR-competent and deficient cell lines. In vitro viability assays show that DFMO and rucaparib cotreatment significantly enhances the cytotoxicity of the chemotherapeutic agent, cisplatin. These results suggest that DFMO may be a useful adjunct chemotherapeutic to improve the anti-tumor efficacy of PARP inhibitors in treating ovarian cancer.


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Average Rating: 5 ★★★★★ (Based on Reviews and 33 reference(s) in Google Scholar.)

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