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Catalog No.: GC40165

C11-BODIPY581/591 is a fluorescent ratio-probe of lipid oxidation.

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C11 BODIPY 581/591 Chemical Structure

Cas No.:217075-36-0

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Sample solution is provided at 25 µL, 10mM.

Product has been cited by 45 publications

Product Documents

Quality Control & SDS

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Preparation of C11 BODIPY 581/591 Working Solution

        1.Preparation of Stock Solution Prepare a 10 mM solution of C11 BODIPY 581/591 in DMSO. Dissolve 1 mg of C11 BODIPY 581/591 in 0.1983 mL of DMSO.

Note: Store the stock solution of C11 BODIPY 581/591 in the dark at -20°C or -80°C in aliquots and use within 2 weeks.

        2.Preparation of Working Solution Dilute the stock solution with pre-warmed serum-free cell culture medium or PBS to obtain a working solution of C11 BODIPY 581/591 at a concentration of 2-10 μM.

Note: Adjust the concentration of the working solution of C11 BODIPY 581/591 according to your experimental needs and use it immediately after preparation.


Cell Staining

        1.Cell Preparation For suspension cells: Collect cells by centrifugation, wash twice with PBS for 5 minutes each time. For adherent cells: Remove the culture medium, digest the cells with trypsin, and collect cells by centrifugation. Discard the supernatant and wash twice with PBS for 5 minutes each time.

        2.Add 1 mL of C11 BODIPY 581/591 working solution and incubate at room temperature for 15 minutes.

        3.Centrifuge at 400 g, 4°C for 3-4 minutes and discard the supernatant.

        4.Wash cells twice with PBS for 5 minutes each time.


           5.1. Resuspend cells in 1 mL of serum-free cell culture medium or PBS and detect by fluorescence microscopy or flow cytometry. When using flow cytometry, excite at 488 nm and 565 nm, measure the signal in the FL1 channel at 505 nm-550 nm, and in the FL2 channel at 580 nm and above. The maximum emission fluorescence of C11 BODIPY 581/591 shifts from 590 nm to around 510 nm when it undergoes redox reaction with reactive oxygen species (ROS) within the cell membrane, and the fluorescence signal is proportional to the production of lipid peroxidation.

          5.2. Take pictures with a fluorescence microscope, using excitation/emission wavelengths of 460–495 nm/510–550 nm for the oxidized form and excitation/emission wavelengths of 565–581 nm/585–591 nm for the reduced form.


This protocol only provides a guideline, and should be modified according to your specific needs.



C11-BODIPY581/591 is an oxidation-sensitive fluorescent fatty acid analogue with fluorescent properties in the red range of the visible spectrum (emission maximum 595 nm), allowing its application in fluorescence microscopy. C11-BODIPY581/591 is easily incorporating into membranes and fluoresces red in the intact state but shifts to green upon free radical-induced oxidation. This characteristic is highly advantageous, it makes the ratio-imaging of oxidant activities at the (sub)cellular level feasible. In addition, the fluorescent properties of C11-BODIPY581/591 allow the use of this probe in fast- and medium- throughput screening of antioxidants in living cells and model membranes in a multiwell/fluorescence reader approach[1][2].

The wavelengths of maximal excitation and emission of fluorophore C11-BODIPY581/591 corresponded to 581 and 591 nm, respectively. Addition of CumOOH/hemin, as an initiator of lipid oxidation, shifted the excitation and emission spectra to shorter wavelengths corresponding to green fluorescence (peak excitation 500 nm, emission 510 nm). C11-BODIPY581/591 is also easily oxidized by other hydroxy-, peroxy- and oxy-radical generating systems such as hydrogen peroxide/Fe2+ and 2,2’-azobis. However, this probe is relatively insensitive to SIN-1, which generates nitric oxide and superoxide[3]

[1]. Drummen GP, et al. C11-BODIPY581/591, an oxidation-sensitive fluorescent lipid peroxidation probe: (micro)spectroscopic characterization and validation of methodology. Free Radic Biol Med. 2002 Aug 15;33(4):473-90.
[2]. Partyka A, et al. Detection of lipid peroxidation in frozen-thawed avian spermatozoa using C11-BODIPY581/591. Theriogenology. 2011 Jun;75(9):1623-9.
[3]. Pap EH, et al. Ratio-fluorescence microscopy of lipid oxidation in living cells using C11-BODIPY581/591. FEBS Lett. 1999 Jun 25;453(3):278-82.

Chemical Properties

Cas No. 217075-36-0 SDF
Chemical Name (T-4)-difluoro[5-[[5-[(1E,3E)-4-phenyl-1,3-butadien-1-yl]-2H-pyrrol-2-ylidene-κN]methyl]-1H-pyrrole-2-undecanoato(2-)-κN1]-borate(1-), monohydrogen
Canonical SMILES [F-][B+3]1([N]2=C(/C=C/C=C/C3=CC=CC=C3)C=CC2=CC4=CC=C(CCCCCCCCCCC([O-])=O)[N-]14)[F-].[H+]
Formula C30H34BF2N2O2 • H M.Wt 504.4
Solubility 30mg/ml in DMSO,Slightly soluble in Methanol Storage Store at -20°C
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

Ginsenoside Rg1 ameliorates sepsis-induced acute kidney injury by inhibiting ferroptosis in renal tubular epithelial cells

J Leukoc Biol 2022 Nov;112(5):1065-1077.PMID:35774015DOI:10.1002/JLB.1A0422-211R.

Acute kidney injury (AKI) represents a prevailing complication of sepsis, and its onset involves ferroptosis. Ginsenoside Rg1 exerts a positive effect on kidney diseases. This study explored the action of ginsenoside Rg1 in sepsis-induced AKI (SI-AKI) by regulating ferroptosis in renal tubular epithelial cells (TECs). Sepsis rat models were established using cecal ligation and puncture (CLP) and cell models were established by treating human renal TECs (HK-2) with LPS to induce ferroptosis. Serum creatinine (SCr) and blood urea nitrogen (BUN) and urine KIM1 contents in rats were determined by ELISA kits. Kidney tissues were subjected to immunohistochemical and H&E stainings. Iron concentration, malondialdehyde (MDA), glutathione (GSH), and ferroptosis-related protein (ferritin light chain [FTL], ferritin heavy chain [FTH], GSH peroxidase 4 [GPX4], and Ferroptosis suppressor protein 1 [FSP1]) levels in kidney tissues and HK-2 cells were measured using ELISA kits and Western blotting. HK-2 cell viability was detected by cell counting kit-8, and cell death was observed via propidium iodide staining. Reactive oxygen species accumulation in cells was detected using C11 BODIPY 581/591 as a molecular probe. In CLP rats, ginsenoside Rg1 reduced SCr, BUN, KIM1, and NGAL levels, thus palliating SI-AKI. Additionally, ginsenoside Rg1 decreased iron content, FTL, FTH, and MDA levels, and elevated GPX4, FSP1, and GSH levels, thereby inhibiting lipid peroxidation and ferroptosis. Moreover, FSP1 knockdown annulled the inhibition of ginsenoside Rg1 on ferroptosis. In vitro experiments, ginsenoside Rg1 raised HK-2 cell viability and lowered iron accumulation and lipid peroxidation during ferroptosis, and its antiferroptosis activity was dependent on FSP1. Ginsenoside Rg1 alleviates SI-AKI, possibly resulting from inhibition of ferroptosis in renal TECs through FSP1.

Tirapazamine suppress osteosarcoma cells in part through SLC7A11 mediated ferroptosis

Biochem Biophys Res Commun 2021 Aug 27;567:118-124.PMID:34147710DOI:10.1016/j.bbrc.2021.06.036.

Osteosarcoma is the most common primary orthopedic malignant bone tumor in adolescents. However, the traditional neoadjuvant chemotherapy regimen has reached the bottleneck. TPZ is a hypoxic prodrug that has a powerful anti-tumor effect in the hypoxic microenvironment of tumors. And ferroptosis is a newly discovered cell death in 2012, and ferroptosis inducers have been used in anti-tumor therapy research in recent decades. Though, the role of TPZ and ferroptosis in osteosarcoma remains unclear. The aim of this study was to investigate the role of TPZ in osteosarcoma and the specific mechanism. MTT assay showed the extraordinary inhibition of TPZ on three osteosarcoma cells under hypoxia. And fluorescence of Fe2+ staining was enhanced by TPZ. Western blotting showed decreased expression of SLC7A11 and GPX4. Lipid peroxidation was confirmed by MDA assay and C11 BODIPY 581/591 staining. SLC7A11 overexpression could restored the proliferation and migration abilities inhibited by TPZ. Thus, we for the first time demonstrated that TPZ could inhibit the proliferation and migration of osteosarcoma cells, and induce ferroptosis in part through inhibiting SLC7A11.

[Carbenoxolone enhances inhibitory effect of RSL3 against cisplatin-resistant testicular cancer cells by promoting ferroptosis]

Nan Fang Yi Ke Da Xue Xue Bao 2022 Mar 20;42(3):405-410.PMID:35426805DOI:10.12122/j.issn.1673-4254.2022.03.13.

Objective: To investigate the inhibitory effect of RSL3 on the proliferation, invasion and migration of cisplatinresistant testicular cancer cells (I-10/DDP) and the effect of carbenoxolone on the activity of RSL3 against testicular cancer. Methods: MTT assay was used to evaluate the survival rate of I-10/DDP cells following treatment with RSL3 (1, 2, 4, 8, 16 or 32 μmol/L) alone or in combination with carbenoxolone (100 μmol/L) or after treatment with Fer-1 (2 μmol/L), RSL3 (4 μmol/L), RSL3+Fer-1, RSL3+carbenoxolone (100 μmol/L), or RSL3+Fer-1+carbenoxolone. Colony formation assay was used to assess the proliferation ability of the treated cells; wounding-healing assay and Transwell assay were used to assess the invasion and migration ability of the cells. The expression of GPX4 was detected using Western blotting, the levels of lipid ROS were detected using C11 BODIPY 581/591 fluorescent probe, and the levels of Fe2+ were determined with FerroOrange fluorescent probe. Results: RSL3 dose-dependently decreased the survival rate of I-10/DDP cells, and the combined treatment with 2, 4, or 8 μmol/L RSL3 with carbenoxolone, as compared with RSL3 treatment alone, resulted in significant reduction of the cell survival rate. The combination with carbenoxolone significantly enhanced the inhibitory effect of RSL3 on colony formation, wound healing rate (P=0.005), invasion and migration of the cells (P < 0.001). Fer-1 obviously attenuated the inhibitory effects of RSL3 alone and its combination with carbenoxolone on I-10/DDP cells (P < 0.01). RSL3 treatment significantly decreased GPX4 expression (P=0.001) and increased lipid ROS level (P=0.001) and Fe2+ level in the cells, and these effects were further enhanced by the combined treatment with carbenoxolone (P < 0.01). Conclusion: Carbenoxolone enhances the inhibitory effect of RSL3 on the proliferation, invasion and migration of cisplatin-resistant testicular cancer cells by promoting RSL3-induced ferroptosis.

Hyperbaric oxygen protects HT22 cells and PC12 cells from damage caused by oxygen-glucose deprivation/reperfusion via the inhibition of Nrf2/System Xc-/GPX4 axis-mediated ferroptosis

PLoS One 2022 Nov 10;17(11):e0276083.PMID:36355759DOI:10.1371/journal.pone.0276083.

This study was to investigate the protective effect of hyperbaric oxygen (HBO) on HT22 and PC12 cell damage caused by oxygen-glucose deprivation/reperfusion-induced ferroptosis. A 2-h oxygen-glucose deprivation and 24-h reperfusion model on HT22 and PC12 cells was used to simulate cerebral ischemia-reperfusion injury. Cell viabilities were detected by Cell Counting Kit-8 (CCK-8) method. The levels of reactive oxygen species (ROS) and lipid reactive oxygen species (Lipid ROS) were detected by fluorescent probes Dihydroethidium (DHE) and C11 BODIPY 581/591. Iron Colorimetric Assay Kit, malondialdehyde (MDA) and glutathione (GSH) activity assay kits were used to detect intracellular iron ion, MDA and GSHcontent. Cell ferroptosis-related ultrastructures were visualized using transmission electron microscopy (TEM). Furthermore, PCR and Western blot analyses were used to detect the expressions of ferroptosis-related genes and proteins. After receiving oxygen-glucose deprivation/reperfusion, the viabilities of HT22 and PC12 cells were significantly decreased; ROS, Lipid ROS, iron ions and MDA accumulation occurred in the cells; GSH contents decreased; TEM showed that cells were ruptured and blebbed, mitochondria atrophied and became smaller, mitochondrial ridges were reduced or even disappeared, and apoptotic bodies appeared. And the expressions of Nrf2, SLC7A11 and GPX4 genes were reduced; the expressions of p-Nrf2/Nrf2, xCT and GPX4 proteins were reduced. Notably, these parameters were significantly reversed by HBO, indicating that HBO can protect HT22 cells and PC12 cells from damage caused by oxygen-glucosedeprivation/reperfusion via the inhibition of Nrf2/System Xc-/GPX4 axis-mediated ferroptosis.

Cinnamtannin B-1, a novel antioxidant for sperm in red deer

Anim Reprod Sci 2018 Aug;195:44-52.PMID:29776697DOI:10.1016/j.anireprosci.2018.05.004.

Cinnamtannin B-1 (CNB-1) is a naturally occurring trimeric A-type proanthocyanidin contained in several plants such as cinnamon (Cinnamomum zeylanicum). It is considered to be a potent antioxidant. The protective effect of CNB-1 against oxidative stress was assessed in red deer epididymal sperm incubated at 37 °C. Cryopreserved sperm from six stags were thawed, pooled and extended to 400 × 106 sperm/ml in BGM (bovine gamete medium). After being aliquoted, the samples were supplemented with different concentrations of CNB-1 (0, 0.1, 1, 10 and 100 μg/mL), with or without induced oxidative stress (100 μM Fe2+/ascorbate). The samples were evaluated after 0, 2 and 4 h of incubation at 37 °C. This experiment was replicated six times. Spermmotility (CASA), viability, mitochondrial membrane potential, acrosomal status, lipoperoxidation (C11 BODIPY 581/591), intracellular reactive oxygen species (ROS) production and DNA status (TUNEL) were assessed. After 4 h of incubation, CNB-1 prevented the deleterious effects of oxidative stress, thus improved sperm progressivity and velocity (P<0.05). Furthermore, 1 and 10 μM CNB-1 improved sperm linearity, even when compared to those samples that had not been subjected to oxidative stress (P<0.05). The greatest concentration, 100 μM, prevented sperm lipoperoxidation and reduced ROS production in samples subjected to oxidative stress.


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