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Catalog No.: GC10395

Dynasore, as a GTPase inhibitor, can rapidly and reversibly inhibit dynamin activity, which prevents endocytosis.

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Dynasore Chemical Structure

Cas No.:304448-55-3

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10mM (in 1mL DMSO)
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Sample solution is provided at 25 µL, 10mM.

Product has been cited by 2 publications

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Cell experiment [1]:

Cell lines

Human OS cell lines (MNNG/HOS, MG-63, and U2-OS)

Preparation Method

Human OS cell lines (MNNG/HOS, MG-63, and U2-OS) were treated with increasing concentrations of dynasore or cisplatin (0 - 100 µM), and then the cell viability was assessed by CCK-8 kit at 24, 48, and 72 h.

Reaction Conditions

0 - 100 µM; at 24, 48, and 72 h


The cell abilities of MNNG/HOS, MG-63, and U2-OS were suppressed in a time- and concentration-dependent manner either treated with dynasore or cisplatin.

Animal experiment [2]:

Animal models

Sprague-Dawley rats

Preparation Method

Sprague-Dawley rats were randomly assigned to sham, SCI, and 1, 10, and 30 mg dynasore groups. The rat model of SCI was established using an established Allen's model. Dynasore was administered via intraperitoneal injection immediately.

Dosage form

1, 10, and 30 mg/kg; i.p.


Results of motor functional test indicated that dynasore ameliorated the motor dysfunction greatly at 3, 7, and 10 days after SCI in rats. Results of western blot showed that dynasore has remarkably reduced the expressions of Drp1, dynamin 1, and dynamin 2 and, moreover, decreased the Bax, cytochrome C, and active Caspase-3 expressions, but increased the expressions of Bcl-2 at 3 days after SCI. Results of immunofluorescent double labeling showed that there were less apoptotic neurons and proliferative astrocytes in the dynasore groups compared with SCI group. Finally, histological assessment via Nissl staining demonstrated that the dynasore groups exhibited a significantly greater number of surviving neurons compared with the SCI group.


[1] Zhong B, et al. Dynasore suppresses cell proliferation, migration, and invasion and enhances the antitumor capacity of cisplatin via STAT3 pathway in osteosarcoma. Cell Death Dis. 2019 Sep 18;10(10):687.

[2] Li G, et al. Dynasore Improves Motor Function Recovery via Inhibition of Neuronal Apoptosis and Astrocytic Proliferation after Spinal Cord Injury in Rats. Mol Neurobiol. 2017 Nov;54(9):7471-7482.


Dynasore, as a GTPase inhibitor, can rapidly and reversibly inhibit dynamin activity, which prevents endocytosis[1].

Dynasore inhibits dynamin GTPase activity and transferrin uptake with IC50 of approximately 15 µM[2]. In vitro, treatment with 80 µM dynasore commonly block dynamin 1 and 2, dynasore also has a potent inhibition on ferroptosis at a range of lower concentrations. Dynasore also potently blocked H2O2-induced cell death at 100 nM[3]. In vitro experiment it demonstrated that treatment with 100 µM dynasore impairs VEGF-induced calcium release[4]. At the ocular surface of ex vivo mouse eyes, 40 uM dynasore blocked stress-stimulated dye uptake. Dynasore is obviously protective of cells and their surface glycocalyx, preventing damage due to oxidative stress, and thus precluding dye entry[5]. In vitro test it exhibited that treatment with 100 µM dynasore rapidly increased the spontaneous EPSC (sEPSC) frequency which was followed by inhibition of both solitary tract-evoked EPSCs (ST-EPSC) as well as asynchronous EPSCs[6]. In peritoneal macrophages and LLC-MK2 cells, treatment with 100 µM dynasore drastically diminished the parasite internalization[7].

In vivo efficacy test it shown that dynasore (10 mg/kg, intraperitoneally) inhibits OS tumorigenesis without inducing nephrotoxicity and hepatotoxicity[8]. In vivo, the ocular mouse Sereny model was administrated 30 mg/kg intraperitoneally did not reduce ocular inflammation, it did provide significant protection against weight loss[9].


[1] Preta G, et al. Dynasore - not just a dynamin inhibitor. Cell Commun Signal. 2015 Apr 10;13:24.

[2] Lee S, et al. Synthesis of potent chemical inhibitors of dynamin GTPase. Bioorg Med Chem Lett. 2010 Aug 15;20(16):4858-64.

[3] Clemente LP, et al. Dynasore Blocks Ferroptosis through Combined Modulation of Iron Uptake and Inhibition of Mitochondrial Respiration. Cells. 2020 Oct 9;9(10):2259.

[4] Webster A, et al. Dynasore protects the ocular surface against damaging oxidative stress. PLoS One. 2018 Oct 10;13(10):e0204288.

[5] Hofmann ME, et al. Dynasore blocks evoked release while augmenting spontaneous synaptic transmission from primary visceral afferents. PLoS One. 2017 Mar 30;12(3):e0174915.

[6] Lum M, et al. Impact of dynasore an inhibitor of dynamin II on Shigella flexneri infection. PLoS One. 2013 Dec 19;8(12):e84975.

[7] Zhong B, et al. Dynasore suppresses cell proliferation, migration, and invasion and enhances the antitumor capacity of cisplatin via STAT3 pathway in osteosarcoma. Cell Death Dis. 2019 Sep 18;10(10):687.

[8] Basagiannis D, et al. Dynasore impairs VEGFR2 signalling in an endocytosis-independent manner. Sci Rep. 2017 Mar 22;7:45035.

[9] Barrias ES, et al. Dynasore, a dynamin inhibitor, inhibits Trypanosoma cruzi entry into peritoneal macrophages. PLoS One. 2010 Jan 20;5(1):e7764.

Chemical Properties

Cas No. 304448-55-3 SDF
Chemical Name (E)-N'-(3,4-dihydroxybenzylidene)-3-hydroxy-2-naphthohydrazide
Canonical SMILES OC1=C(C(N/N=C/C(C=C2)=CC(O)=C2O)=O)C=C(C=CC=C3)C3=C1
Formula C18H14N2O4 M.Wt 322.31
Solubility ≥ 16.12mg/mL in DMSO 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

Dynasore, a cell-permeable inhibitor of dynamin

Dynamin is essential for clathrin-dependent coated vesicle formation. It is required for membrane budding at a late stage during the transition from a fully formed pit to a pinched-off vesicle. Dynamin may also fulfill other roles during earlier stages of vesicle formation. We have screened about 16,000 small molecules and have identified 1, named here dynasore, that interferes in vitro with the GTPase activity of dynamin1, dynamin2, and Drp1, the mitochondrial dynamin, but not of other small GTPases. Dynasore acts as a potent inhibitor of endocytic pathways known to depend on dynamin by rapidly blocking coated vesicle formation within seconds of dynasore addition. Two types of coated pit intermediates accumulate during dynasore treatment, U-shaped, half formed pits and O-shaped, fully formed pits, captured while pinching off. Thus, dynamin acts at two steps during clathrin coat formation; GTP hydrolysis is probably needed at both steps.

Dynasore Blocks Ferroptosis through Combined Modulation of Iron Uptake and Inhibition of Mitochondrial Respiration

Ferroptosis is a form of regulated necrosis characterized by a chain-reaction of detrimental membrane lipid peroxidation following collapse of glutathione peroxidase 4 (Gpx4) activity. This lipid peroxidation is catalyzed by labile ferric iron. Therefore, iron import mediated via transferrin receptors and both, enzymatic and non-enzymatic iron-dependent radical formation are crucial prerequisites for the execution of ferroptosis. Intriguingly, the dynamin inhibitor dynasore, which has been shown to block transferrin receptor endocytosis, can protect from ischemia/reperfusion injury as well as neuronal cell death following spinal cord injury. Yet, it is unknown how dynasore exerts these cell death-protective effects. Using small interfering RNA suppression, lipid reactive oxygen species (ROS), iron tracers and bona fide inducers of ferroptosis, we find that dynasore treatment in lung adenocarcinoma and neuronal cell lines strongly protects these from ferroptosis. Surprisingly, while the dynasore targets dynamin 1 and 2 promote extracellular iron uptake, their silencing was not sufficient to block ferroptosis suggesting that this route of extracellular iron uptake is dispensable for acute induction of ferroptosis and dynasore must have an additional off-target activity mediating full ferroptosis protection. Instead, in intact cells, dynasore inhibited mitochondrial respiration and thereby mitochondrial ROS production which can feed into detrimental lipid peroxidation and ferroptotic cell death in the presence of labile iron. In addition, in cell free systems, dynasore showed radical scavenger properties and acted as a broadly active antioxidant which is superior to N-acetylcysteine (NAC) in blocking ferroptosis. Thus, dynasore can function as a highly active inhibitor of ROS-driven types of cell death via combined modulation of the iron pool and inhibition of general ROS by simultaneously blocking two routes required for ROS and lipid-ROS driven cell death, respectively. These data have important implications for the interpretation of studies observing tissue-protective effects of this dynamin inhibitor as well as raise awareness that off-target ROS scavenging activities of small molecules used to interrogate the ferroptosis pathway should be taken into consideration.

Dynasore - not just a dynamin inhibitor

Dynamin is a GTPase protein that is essential for membrane fission during clathrin-mediated endocytosis in eukaryotic cells. Dynasore is a GTPase inhibitor that rapidly and reversibly inhibits dynamin activity, which prevents endocytosis. However, comparison between cells treated with dynasore and RNA interference of genes encoding dynamin, reveals evidence that dynasore reduces labile cholesterol in the plasma membrane, and disrupts lipid raft organization, in a dynamin-independent manner. To explore the role of dynamin it is important to use multiple dynamin inhibitors, alongside the use of dynamin mutants and RNA interference targeting genes encoding dynamin. On the other hand, dynasore provides an interesting tool to explore the regulation of cholesterol in plasma membranes.

Mitochondrial dynamics in type 2 diabetes: Pathophysiological implications

Mitochondria play a key role in maintaining cellular metabolic homeostasis. These organelles have a high plasticity and are involved in dynamic processes such as mitochondrial fusion and fission, mitophagy and mitochondrial biogenesis. Type 2 diabetes is characterised by mitochondrial dysfunction, high production of reactive oxygen species (ROS) and low levels of ATP. Mitochondrial fusion is modulated by different proteins, including mitofusin-1 (MFN1), mitofusin-2 (MFN2) and optic atrophy (OPA-1), while fission is controlled by mitochondrial fission 1 (FIS1), dynamin-related protein 1 (DRP1) and mitochondrial fission factor (MFF). PARKIN and (PTEN)-induced putative kinase 1 (PINK1) participate in the process of mitophagy, for which mitochondrial fission is necessary. In this review, we discuss the molecular pathways of mitochondrial dynamics, their impairment under type 2 diabetes, and pharmaceutical approaches for targeting mitochondrial dynamics, such as mitochondrial division inhibitor-1 (mdivi-1), dynasore, P110 and 15-oxospiramilactone. Furthermore, we discuss the pathophysiological implications of impaired mitochondrial dynamics, especially in type 2 diabetes.

Dynasore potentiates c-Met inhibitors against hepatocellular carcinoma through destabilizing c-Met

c-Met receptor is frequently overexpressed in hepatocellular carcinoma and thus considered as an attractive target for pharmacological intervention with small molecule tyrosine kinase inhibitors. Albeit with the development of multiple c-Met inhibitors, none reached clinical application in the treatment of hepatoma so far. To improve the efficacy of c-Met inhibitors towards hepatocellular carcinoma, we investigated the combined effects of the dynamin inhibitor dynasore with several c-Met inhibitors, including tivantinib, PHA-665752, and JNJ-38877605. We provide several lines of evidence that dynasore enhanced the inhibitory effects of these inhibitors on hepatoma cell proliferation and migration, accompanied with increased cell cycle arrest and apoptosis. Mechanically, the combinatorial treatments decreased c-Met levels and hence markedly disrupted downstream signaling, as revealed by the dramatically declined phosphorylation of AKT and MEK. Taken together, our findings demonstrate that the candidate agent dynasore potentiated the inhibitory effects of c-Met inhibitors against hepatoma cells and will shed light on the development of novel therapeutic strategies to target c-Met in the clinical management of hepatocellular carcinoma patients.


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Average Rating: 5 ★★★★★ (Based on Reviews and 37 reference(s) in Google Scholar.)

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