| Size | Price | Stock | Qty |
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| 1mg |
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| 100mg | |||
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| Targets |
The primary molecular target of Latrunculin B is monomeric globular actin (G-actin). The compound binds directly to G-actin in a 1:1 stoichiometric ratio, forming a stable complex that sequesters actin monomers and prevents their assembly into filamentous actin (F-actin). The binding affinity of Latrunculin B for G-actin is characterized by an IC50 of approximately 60 nM in the absence of serum. By binding to G-actin, Latrunculin B effectively shifts the equilibrium between the globular and filamentous forms of actin toward the monomeric state, leading to the depolymerization of existing actin filaments and the inhibition of new filament formation. Unlike cytochalasins, which cap the barbed ends of actin filaments, Latrunculin B acts by sequestering actin monomers, providing a distinct mechanism of actin disruption. The compound's interaction with actin is reversible upon washout, making it useful for transient disruption studies.
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| ln Vitro |
HeLa cells are growth inhibited by latrunculin B, with an IC50 value of 1.4 μM[1]. Pulmonary vein cardiomyocytes' electrical properties and arrhythmogenesis are regulated by latrunculin B. In preparations of pulmonary veins (PV), latrunculin B (100 nM) decreases spontaneous electrical activity by 16±4%. In PV cardiomyocytes, latrunculin B (100 nM) decreases stretch-activated BKCa currents, late Na+ currents, L-type Ca2+ currents, and Na+/Ca2+ exchange currents. In isolated PV cardiomyocytes, latrunculin B boosted delayed rectifier K+ current but decreased transient outward K+ current and ultrafast delayed rectifier K+ current. In PV cardiomyocytes, latrunculin B (100 nM) lowers the amount of transient Ca2+ and sarcoplasmic reticulum Ca2+. Stretch-induced increases in spontaneous electrical activity and triggered activity are attenuated by latrunculin B [2].
In vitro, Latrunculin B causes concentration-dependent disruption of actin organization in cultured cells. Treatment with the compound leads to the loss of stress fibers, changes in cell shape, and the formation of actin aggregates or puncta. The disruption of the actin cytoskeleton impairs a wide range of cellular processes that depend on actin dynamics, including cell migration, cytokinesis, endocytosis, and intracellular trafficking. In cell-free systems, Latrunculin B inhibits the polymerization of purified G-actin into F-actin, as measured by various biochemical assays. The compound is effective at nanomolar concentrations in the absence of serum, but its potency is significantly reduced in the presence of serum proteins, with an IC50 of approximately 900 nM in serum-containing media. This reduction in potency is attributed to binding of the compound to serum proteins, which limits its free concentration and cellular uptake. Despite this, Latrunculin B remains active in cell culture at appropriate concentrations. |
| ln Vivo |
In vivo, Latrunculin B has been extensively used to study actin-dependent processes in various model organisms, including zebrafish, Xenopus, and Drosophila. In zebrafish embryos, the compound is administered by immersion in the tank water or by microinjection to disrupt actin dynamics during development. It has been used to study the role of the actin cytoskeleton in gastrulation, neural crest cell migration, angiogenesis, and wound healing. For example, low concentrations of Latrunculin B have been used in transgenic zebrafish lines expressing fluorescent actin reporters to investigate the functional importance of filopodia in endothelial cell guidance during angiogenesis. In mouse models, Latrunculin B has been applied topically or injected locally to study tissue morphogenesis and repair. The compound has also been shown to modulate pulmonary vein electrophysiological characteristics and attenuate the development of stretch arrhythmias, suggesting potential applications in cardiac electrophysiology research. Additionally, Latrunculin B exhibits antifungal and antiprotozoal activity, which may contribute to its biological effects in certain experimental contexts.
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| Enzyme Assay |
The non-cellular assay for Latrunculin B involves the measurement of actin polymerization inhibition using purified G-actin and a fluorescence-based readout. In a typical assay, pyrene-labeled G-actin is incubated with varying concentrations of Latrunculin B in polymerization buffer containing salts and ATP. Polymerization is initiated by the addition of Mg²⁺ and KCl, and the increase in pyrene fluorescence (which occurs upon actin polymerization) is monitored over time using a fluorescence spectrophotometer. The extent of polymerization inhibition is calculated as the decrease in the rate or final extent of fluorescence increase relative to untreated controls. The IC50 value is determined from concentration-response curves. In the presence of serum or actin-binding proteins, the potency of Latrunculin B may be reduced, and assays are often performed in serum-free conditions to obtain accurate potency measurements. The specificity of Latrunculin B for actin over other cytoskeletal proteins can be confirmed by showing that it does not affect tubulin polymerization or other non-actin cellular processes at relevant concentrations.
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| Cell Assay |
The cellular assay for Latrunculin B typically uses cultured mammalian cells, such as fibroblasts, endothelial cells, or epithelial cells. Cells are seeded on coverslips or in multi-well plates and allowed to adhere and spread. Latrunculin B is added to the culture medium at various concentrations (typically 0.1-10 μM) for defined time periods (ranging from minutes to hours). After treatment, cells are fixed with paraformaldehyde and permeabilized with Triton X-100. The actin cytoskeleton is visualized by fluorescent staining with phalloidin conjugated to a fluorophore (e.g., FITC, TRITC, or Alexa Fluor), which binds specifically to F-actin. Cells are then examined by fluorescence microscopy to assess changes in actin organization, such as the loss of stress fibers, cortical actin disruption, and the formation of actin aggregates. In some experiments, cells are co-stained with antibodies against other cytoskeletal components or with markers of specific cellular structures to study the effects of actin disruption on overall cell architecture. Quantitative analysis of actin filament content can be performed by measuring phalloidin fluorescence intensity using flow cytometry or image analysis software. Cell viability is assessed using standard assays to ensure that the observed cytoskeletal changes are not due to cytotoxicity.
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| Animal Protocol |
The in vivo animal studies involving Latrunculin B vary depending on the model organism and experimental question. In zebrafish, embryos are typically treated by adding Latrunculin B directly to the embryo medium at concentrations ranging from 1-10 μM. The compound is allowed to diffuse through the chorion and into the embryo tissues. Treated embryos are observed under a stereomicroscope or confocal microscope to assess developmental defects, such as gastrulation failure, abnormal cell migration, or vascular malformations. In some studies, Latrunculin B is microinjected into specific tissues or cells at defined developmental stages to achieve localized disruption of actin dynamics. In mouse models, the compound is often administered by subcutaneous injection, intraperitoneal injection, or topical application to the skin or other tissues. Dosages and treatment schedules are optimized based on the specific experimental endpoints. In wound healing studies, Latrunculin B may be applied to excisional wounds to study the role of actin polymerization in keratinocyte migration and re-epithelialization. In cardiac electrophysiology studies, the compound is perfused over isolated heart preparations or injected into the pulmonary vein to study its effects on arrhythmogenesis.
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| ADME/Pharmacokinetics |
Latrunculin B exhibits moderate cell permeability and is soluble in DMSO at concentrations up to 25 mg/mL. However, its inhibitory effect is rapidly diminished in serum-containing media due to binding to serum proteins, and its potency is significantly lower in the presence of serum (IC50 ~900 nM) compared to serum-free conditions (IC50 ~60 nM). The compound is typically stored as a stock solution in DMSO at -20°C, protected from light, to prevent degradation. Latrunculin B is stable in DMSO for extended periods when stored properly. For in vivo applications, the compound may require formulation with appropriate vehicles to ensure adequate bioavailability and tissue distribution. The compound's pharmacokinetic properties are not well-characterized due to its primary use as a research tool rather than a therapeutic agent.
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| Toxicity/Toxicokinetics |
Latrunculin B is considered to have low acute toxicity at typical working concentrations in vitro. However, as a potent cytoskeletal disruptor, it can be toxic to cells at higher concentrations or with prolonged exposure, leading to cell detachment and death. The effects of Latrunculin B are reversible upon washout, as the compound dissociates from G-actin, allowing actin polymerization to resume. In animal studies, the compound is generally well-tolerated at the doses used for acute experiments, but repeated or high-dose administration may cause adverse effects due to widespread disruption of the actin cytoskeleton in multiple tissues. Latrunculin B should be handled with appropriate personal protective equipment, as it is a bioactive marine toxin. It is not approved for human use and is strictly a research reagent.
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| References |
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| Additional Infomation |
Latrunculin B is a macrocyclic lactone consisting of a 14-membered bicyclic lactone ring linked to a rare 2-thiazolidinone moiety. It was extracted from the Red Sea sponge Latrunculia magnifica. It functions as a metabolite, an actin polymerization inhibitor, and a toxin. It is a macrocyclic lactone, cyclic hemiacetal, oxabicycloalkane, and thiazolidinone. Latrunculin B is a 14-membered macrocyclic lactone with a 2-thiazolidinone moiety, isolated from the Red Sea sponge Latrunculia magnifica. Latrunculin B has been reported in Brassica napus, Arabidopsis quadricolor, and several other organisms with relevant data.
Latrunculin B is a widely used research tool in cell biology and has contributed significantly to our understanding of actin dynamics and cytoskeletal function. It is slightly less potent than Latrunculin A but exhibits comparable short-term efficacy and is often preferred for certain applications due to differences in solubility or cellular uptake. The compound's transient mode of action makes it particularly useful for short-duration cellular studies investigating rapid actin dynamics, such as cell motility, phagocytosis, and membrane trafficking. In addition to its role in basic research, Latrunculin B has been investigated for potential therapeutic applications, including the treatment of glaucoma, based on its ability to modulate actin dynamics in the trabecular meshwork and lower intraocular pressure. However, its clinical development has been limited by its toxicity and lack of target specificity. |
| Molecular Formula |
C20H29NO5S
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|---|---|
| Molecular Weight |
395.51
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| Exact Mass |
395.177
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| CAS # |
76343-94-7
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| PubChem CID |
6436219
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| Appearance |
Colorless to off-white solid powder
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| LogP |
3.632
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
6
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| Rotatable Bond Count |
1
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| Heavy Atom Count |
27
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| Complexity |
634
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| Defined Atom Stereocenter Count |
5
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| SMILES |
C[C@H]/1CC[C@@H]2C[C@H](C[C@@](O2)([C@@H]3CSC(=O)N3)O)OC(=O)/C=C(\CC/C=C1)/C
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| InChi Key |
NSHPHXHGRHSMIK-JRIKCGFMSA-N
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| InChi Code |
InChI=1S/C20H29NO5S/c1-13-5-3-4-6-14(2)9-18(22)25-16-10-15(8-7-13)26-20(24,11-16)17-12-27-19(23)21-17/h3,5,9,13,15-17,24H,4,6-8,10-12H2,1-2H3,(H,21,23)/b5-3-,14-9-/t13-,15-,16-,17+,20-/m1/s1
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| Chemical Name |
(4R)-4-[(1R,4Z,8Z,10S,13R,15R)-15-hydroxy-5,10-dimethyl-3-oxo-2,14-dioxabicyclo[11.3.1]heptadeca-4,8-dien-15-yl]-1,3-thiazolidin-2-one
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| Synonyms |
LATB; LAT-B; Latrunculin B
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.5284 mL | 12.6419 mL | 25.2838 mL | |
| 5 mM | 0.5057 mL | 2.5284 mL | 5.0568 mL | |
| 10 mM | 0.2528 mL | 1.2642 mL | 2.5284 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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