Psammaplin A
Based on 1 Customer Validation
Psammaplin A is a marine metabolite. Psammaplin A is a selective HDAC1 (IC50: 45 nM), DNA methyltransferases (IC50: 18.6 nM) and aminopeptidase N (APN) (IC50: 18 μM) inhibitor. Psammaplin A also inhibits DNA topoisomerase and farnesyl protein transferase. Psammaplin A is a PPARγ activator and induces apoptosis. Psammaplin A has antitumor and anti-inflammatory activities. Psammaplin A has antibacterial activity against Gram-positive bacteria and inhibits DNA synthesis and DNA gyrase activity. Psammaplin A inhibits angiogenesis.
For research use only. We do not sell to patients.
- Purity : 96.0%
- CAS No.: 110659-91-1
- Formula: C22H24Br2N4O6S2
- Molecular Weight:664.39
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Storage:
4°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
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Biological Activity
Description
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HDAC1 45 nM (IC50) |
DNA Methyltransferase 18.6 nM (IC50) |
PPARγ |
APN 18 μM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| A549 | ED50 |
0.57 μg/mL
Compound: 1
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Cytotoxicity against human A549 cells
Cytotoxicity against human A549 cells
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[PMID: 14640526] |
| A549 | GI50 |
4.5 μM
Compound: Psammaplin A
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Cytotoxicity against human A549 cells assessed as reduction in cell growth inhibition after 96 hrs by MTT assay
Cytotoxicity against human A549 cells assessed as reduction in cell growth inhibition after 96 hrs by MTT assay
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[PMID: 27460171] |
| A549 | GI50 |
7.5 μM
Compound: 11c
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Growth inhibition of human A549 cells after 96 hrs by sulphorhodamine B assay
Growth inhibition of human A549 cells after 96 hrs by sulphorhodamine B assay
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[PMID: 22280363] |
| A549 | IC50 |
1.18 μM
Compound: 1, PsA
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Cytotoxicity against human A549 cells by SRB assay
Cytotoxicity against human A549 cells by SRB assay
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[PMID: 25884112] |
| A549 | IC50 |
1.76 μM
Compound: PsA
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Cytotoxicity against human A549 cells assessed as reduction in cell viability by SRB assay
Cytotoxicity against human A549 cells assessed as reduction in cell viability by SRB assay
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[PMID: 33636429] |
| CHO-K1 | EC50 |
0.9 μM
Compound: 4
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Cytotoxicity against CHO-K1 cells by Alamar blue assay
Cytotoxicity against CHO-K1 cells by Alamar blue assay
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[PMID: 16962325] |
| HCT-116 | IC50 |
0.61 μM
Compound: PsA
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Cytotoxicity against human HCT-116 cells assessed as reduction in cell viability by SRB assay
Cytotoxicity against human HCT-116 cells assessed as reduction in cell viability by SRB assay
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[PMID: 33636429] |
| HCT-116 | IC50 |
1.62 μM
Compound: 1, PsA
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Cytotoxicity against human HCT116 cells by SRB assay
Cytotoxicity against human HCT116 cells by SRB assay
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[PMID: 25884112] |
| HCT-116 | IC50 |
3.05 μM
Compound: PsA
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Antiproliferative activity against human HCT-116 cells incubated for 48 hrs by MTT assay
Antiproliferative activity against human HCT-116 cells incubated for 48 hrs by MTT assay
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[PMID: 38851056] |
| HCT-15 | ED50 |
0.68 μg/mL
Compound: 1
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Cytotoxicity against human HCT15 cells
Cytotoxicity against human HCT15 cells
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[PMID: 14640526] |
| HeLa | IC50 |
0.05 μM
Compound: Psammaplin A
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Inhibition of HDAC in human HeLa cells using Fluor deLys as substrate assessed as deacetylation of substrate by fluorescence assay
Inhibition of HDAC in human HeLa cells using Fluor deLys as substrate assessed as deacetylation of substrate by fluorescence assay
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[PMID: 27460171] |
| HL-60 | GI50 |
0.29 μM
Compound: Psammaplin A
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Cytotoxicity against human HL60 cells assessed as reduction in cell growth inhibition after 72 hrs by trypan blue-staining based hemocytometric analysis
Cytotoxicity against human HL60 cells assessed as reduction in cell growth inhibition after 72 hrs by trypan blue-staining based hemocytometric analysis
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[PMID: 27460171] |
| HL-60 | GI50 |
0.37 μM
Compound: 1; PsA
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Growth inhibition of human HL-60 cells after 72 hrs by trypan blue dye based assay
Growth inhibition of human HL-60 cells after 72 hrs by trypan blue dye based assay
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[PMID: 33488962] |
| MCF7 | EC50 |
5.7 μM
Compound: 1
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Activation of PPARgamma transfected in human MCF7 cells by luciferase reporter gene assay
Activation of PPARgamma transfected in human MCF7 cells by luciferase reporter gene assay
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[PMID: 16643023] |
| MCF7 | GI50 |
1.27 μM
Compound: 11c
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Growth inhibition of human MCF7 cells after 96 hrs by sulphorhodamine B assay
Growth inhibition of human MCF7 cells after 96 hrs by sulphorhodamine B assay
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[PMID: 22280363] |
| MCF7 | GI50 |
2.26 μM
Compound: Psammaplin A
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Cytotoxicity against human MCF7 cells assessed as reduction in cell growth inhibition after 96 hrs by MTT assay
Cytotoxicity against human MCF7 cells assessed as reduction in cell growth inhibition after 96 hrs by MTT assay
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[PMID: 27460171] |
| MCF7 | IC50 |
5 μM
Compound: 1
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Antiproliferative activity against human MCF7 cells by neutral red method
Antiproliferative activity against human MCF7 cells by neutral red method
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[PMID: 16643023] |
| MDA-MB-231 | IC50 |
1.31 μM
Compound: PsA
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Cytotoxicity against human MDA-MB-231 cells assessed as reduction in cell viability by SRB assay
Cytotoxicity against human MDA-MB-231 cells assessed as reduction in cell viability by SRB assay
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[PMID: 33636429] |
| P388 | IC50 |
0.3 μg/mL
Compound: 9
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Cytotoxicity against mouse P388 cells assessed as cell growth inhibition
Cytotoxicity against mouse P388 cells assessed as cell growth inhibition
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[PMID: 34826681] |
| PC-3 | GI50 |
3.52 μM
Compound: Psammaplin A
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Cytotoxicity against human PC3 cells assessed as reduction in cell growth inhibition after 96 hrs by MTT assay
Cytotoxicity against human PC3 cells assessed as reduction in cell growth inhibition after 96 hrs by MTT assay
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[PMID: 27460171] |
| SK-HEP1 | IC50 |
1.29 μM
Compound: PsA
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Cytotoxicity against human SK-HEP1 cells assessed as reduction in cell viability by SRB assay
Cytotoxicity against human SK-HEP1 cells assessed as reduction in cell viability by SRB assay
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[PMID: 33636429] |
| SK-MEL-2 | ED50 |
0.13 μg/mL
Compound: 1
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Cytotoxicity against human SK-MEL-2 cells
Cytotoxicity against human SK-MEL-2 cells
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[PMID: 14640526] |
| SK-OV-3 | ED50 |
0.14 μg/mL
Compound: 1
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Cytotoxicity against human SKOV3 cells
Cytotoxicity against human SKOV3 cells
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[PMID: 14640526] |
| SNU-638 | IC50 |
0.56 μM
Compound: PsA
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Cytotoxicity against human SNU-638 cells assessed as reduction in cell viability by SRB assay
Cytotoxicity against human SNU-638 cells assessed as reduction in cell viability by SRB assay
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[PMID: 33636429] |
| T-cell | EC50 |
0.2 μM
Compound: Psammaplin A
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Reactivation of latent HIV1 NL4-3-Luc expression in human naive CD4+ T cells treated 7 days post-infection measured after 48 hrs by luminescence plate reader analysis
Reactivation of latent HIV1 NL4-3-Luc expression in human naive CD4+ T cells treated 7 days post-infection measured after 48 hrs by luminescence plate reader analysis
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[PMID: 24495105] |
| WI-38 | GI50 |
3.44 μM
Compound: 11c
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Growth inhibition of human WI38 cells after 96 hrs by sulphorhodamine B assay
Growth inhibition of human WI38 cells after 96 hrs by sulphorhodamine B assay
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[PMID: 22280363] |
| XF498 | ED50 |
0.57 μg/mL
Compound: 1
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Cytotoxicity against human XF498 cells
Cytotoxicity against human XF498 cells
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[PMID: 14640526] |
In Vitro
Psammaplin A inhibits the viability of A549 (GI50: 7.5 μM), MCF7 (GI50: 1.27 μM), and WI38 (GI50: 3.44 μM) cells[1].
Psammaplin A (72 h) inhibits the viability of A549 (IC50: 1.18 μM) and HCT116 (IC50: 1.62 μM) cells[2].
Psammaplin A (0.5-5 μM) inhibits bFGF-induced angiogenesis in bovine aortic endothelial cells (BAEC) in a dose-dependent manner[3].
Psammaplin A (0-100 μg/mL, 1-4 h) inhibits the toxicity of INT-407 cells induced by V. vulnificus in a concentration- and time-dependent manner[4].
Psammaplin A (0-100 μg/mL, 0-13 h) inhibits the growth of V. vulnificus in a concentration-dependent manner[4].
Psammaplin A (0-40 μM, 12 h) inhibits the viability of the macrophage cell line RAW264.7 in a concentration-dependent manner[6].
Psammaplin A (0-500 μM, 2 h) inhibits SV40 DNA replication in HeLa cells in a concentration-dependent manner.
Psammaplin A (125-500 μM, 30 min) inhibits the catalytic activity of topoisomerase I[6].
Psammaplin A (125-500 μM, 15 min) inhibits the binding activity of RPA to single-stranded DNA[6].
Psammaplin A (1-40 μM, 30 min) inhibits the activity of polymerase α-primase in a concentration-dependent manner[6].
Psammaplin A (3-30 μM, 4-16 h) induces apoptosis in T47D and MCF-7 cells[8].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:MCF7 cells
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Concentration:5 μM
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Incubation Time:24 h
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Result:Up-regulated the expression of Ac-H3 protein.
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Cell Line:INT-407 cells
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Concentration:0, 12.5, 25, 50, 100 μg/mL
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Incubation Time:1, 2, 3, 4 h
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Result:Reduced cytotoxicity.
Reduced cell damage.
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Cell Line:Macrophage cell line RAW 264.7
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Concentration:0, 1, 5, 10, 20, 40 μM
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Incubation Time:12 h
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Result:Reduced the number of viable cells.
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Cell Line:MCF-7 and T47D cells
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Concentration:3, 10, 30 μM
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Incubation Time:4, 8, 16 h
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Result:Increased cells apoptosis.
In Vivo
Psammaplin A (5-50 μg, i.p., once) improves the survival rate of mice in the V. vulnificus-infected model[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:A549 cell-implanted xenograft model (male athymic BALB/c mice, 6 weeks old, 18-20 g)[2]
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Dosage:30 mg/kg
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Administration:Intraperitoneal injection (i.p.), three times a week for 35 d
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Result:Inhibited the tumor growth.
Inhibited the expression of the proliferation biomarker Ki-67 in both central and edge region of tumor tissues.
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Animal Model:V. vulnificus-infected model (35 female ICR mice, 8 weeks old, 20-22 g)[4]
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Dosage:5, 10, 25 and 50 μg
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Administration:Intraperitoneal injection (i.p.), once
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Result:Prolonged survival time of mice.
Inhibited damage to the intestines, liver and spleen of mice.
Chemical Information
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CAS No. 110659-91-1
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Appearance Solid
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Molecular Weight 664.39
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Formula C22H24Br2N4O6S2
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Color Off-white to yellow
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SMILES
O=C(NCCSSCCNC(/C(CC1=CC(Br)=C(O)C=C1)=N/O)=O)/C(CC2=CC(Br)=C(O)C=C2)=N/O
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Solvent & Solubility
In Vitro:
DMSO : 33.3 mg/mL (50.12 mM; Need ultrasonic and warming; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (stored under nitrogen). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (stored under nitrogen). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Protocols
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
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Human pluripotent stem cell endothelial-cell differentiation
Human pluripotent stem cell endothelial differentiation is based on stepwise developmental patterning: early activation of WNT/GSK3β inhibition promotes mesodermal or vascular progenitor entry, followed by endothelial specification using VEGF-related signaling, BMP4, FGF2, Notch modulation, or cAMP depending on the published protocol. Endothelial differentiation is read out by acquisition of CD31, CD34, VE-cadherin/CD144, KDR/VEGFR2, vWF, Tie2, NOS3, acetylated LDL uptake, tube/network formation, barrier function, and in vivo vessel-forming capacity where tested.
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Vascular/Branching Fractal Analysis
Vascular/branching fractal analysis quantifies the geometric complexity of vessel trees or vascular networks from segmented 2D images, commonly by converting vessels into binary and/or skeletonized maps and estimating fractal dimension using box-counting or related approaches. Fractal dimension is interpreted as an image-derived readout of vascular branching complexity, space filling, or density, and has been applied to retinal photographs, fluorescein angiography, OCT angiography, capillary perfusion maps, and in vitro Matrigel angiogenesis networks. The assay readout is generated from vessel-positive pixels after image preprocessing, vessel segmentation, binarization, and optional skeletonization; reported outputs include fractal dimension, vessel density, branchpoint density, endpoint density, vessel length density, tortuosity, and generation-based branching metrics when VESGEN-style analysis is used. The biological interpretation is limited to quantitative vascular patterning and s
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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BrdU Incorporation Assay
Bromodeoxyuridine (BrdU) incorporation assay is based on the principle that BrdU, a thymidine analog, is incorporated into newly synthesized DNA during the S phase of the cell cycle, thereby serving as a marker of DNA replication and cellular proliferation. Incorporated BrdU can be detected using anti-BrdU antibodies following DNA denaturation, enabling visualization or quantification of proliferating cells through immunochemical detection methods such as immunofluorescence or immunohistochemistry.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Gram Staining of Tissue Sections
Gram staining of tissue sections is a histochemical technique used to differentiate Gram-positive and Gram-negative bacteria within histological specimens based on differences in bacterial cell wall structure and dye retention, adapted from classical bacteriological Gram staining into tissue-compatible “histological Gram stain” variants. In tissue applications, modifications of the Brown-Hopps and Brown-Brenn methods are commonly used to improve differentiation of microorganisms embedded within host connective tissue and to reduce overstaining or loss of Gram-negative signal, which are known limitations of earlier approaches. The principle relies on crystal violet-iodine complex retention in Gram-positive organisms and subsequent decolorization and counterstaining steps that allow contrast visualization of Gram-negative organisms against tissue background.
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Bacterial live/dead nucleic-acid viability staining
The LIVE/DEAD bacterial viability staining method is based on differential permeability of nucleic-acid-binding fluorescent dyes, most commonly SYTO 9 and propidium iodide (PI), which enables discrimination of bacterial populations with intact versus compromised cytoplasmic membranes. SYTO 9 penetrates both intact and damaged bacterial membranes and binds nucleic acids to produce green fluorescence, whereas propidium iodide penetrates only cells with compromised membranes and fluoresces red while also reducing SYTO 9 signal through competitive binding and fluorescence interactions. The resulting fluorescence pattern is interpreted as a proxy for membrane integrity, which is widely used as an indicator of bacterial viability in microscopy, flow cytometry, and spectroscopic platforms. However, mechanistic studies show that SYTO 9 and PI interactions involve displacement and fluorescence resonance energy transfer effects, which can influence signal interpretation depending on dye ratios a
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EdU Incorporation Assay (Click Chemistry-Based DNA Synthesis Measurement)
The EdU incorporation assay measures DNA synthesis by adding the thymidine analog 5-ethynyl-2′-deoxyuridine to cells or tissues, where it is incorporated into newly synthesized DNA during S phase. Incorporated EdU is detected by copper-catalyzed azide-alkyne cycloaddition, in which a fluorescent azide covalently reacts with the ethynyl group on EdU, allowing S-phase cells to be detected by fluorescence microscopy, flow cytometry, or high-content imaging. EdU detection does not require DNA denaturation or anti-BrdU antibody access, which preserves sample structure and improves compatibility with immunostaining and multiparameter cytometry compared with BrdU-based detection. EdU can be cytotoxic in a cell-type- and exposure-dependent manner, so pulse duration, concentration, and continuous-labeling designs should be validated for each cell type.
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Endothelial Tube Formation Assay
Endothelial tube formation assay evaluates the ability of endothelial cells to attach, migrate, align, and organize into capillary-like networks when cultured on gelled basement membrane extract or Matrigel; the readout is the morphology and quantity of tube-like networks, which reflects an in vitro endothelial morphogenesis step related to angiogenesis. Basement membrane extract/Matrigel provides laminin-rich extracellular matrix cues that support endothelial differentiation into capillary-like structures, but it can contain biologically active growth factors, so growth-factor-reduced matrix is preferred when testing defined angiogenic stimulators or inhibitors.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Endothelial Cell Migration/Angiogenic Sprouting Assay
Endothelial cell migration and angiogenic sprouting assays are in vitro (and partially ex vivo-adapted) functional models that quantify the ability of endothelial cells to undergo coordinated migration, extracellular matrix invasion, and multicellular organization into capillary-like sprouts in response to pro-angiogenic stimuli such as VEGF, bFGF, or conditioned microenvironments. These assays are used to model early angiogenic events including tip-cell formation, directional migration, and lumen-like sprout extension, which collectively reflect angiogenic activation and vascular morphogenesis processes observed in vivo.
Purity & Documentation
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Data Sheet (277 KB)
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SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
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Handling Instructions (2659 KB)
References
[1]. Baud MG, et al. Defining the mechanism of action and enzymatic selectivity of psammaplin A against its epigenetic targets. J Med Chem. 2012 Feb 23;55(4):1731-50. [Content Brief]
[2]. Hong S, et al. Efficient synthesis and biological activity of Psammaplin A and its analogues as antitumor agents. Eur J Med Chem. 2015;96:218-30. [Content Brief]
[3]. Shim JS, et al. Psammaplin A, a marine natural product, inhibits aminopeptidase N and suppresses angiogenesis in vitro. Cancer Lett. 2004 Jan 20;203(2):163-9. [Content Brief]
[4]. Lee BC, et al. In vitro and in vivo anti-Vibrio vulnificus activity of psammaplin A, a natural marine compound. Mol Med Rep. 2016 Sep;14(3):2691-6. [Content Brief]
[5]. Piña IC, et al. Psammaplins from the sponge Pseudoceratina purpurea: inhibition of both histone deacetylase and DNA methyltransferase. J Org Chem. 2003 May 16;68(10):3866-73. [Content Brief]
[6]. Jiang Y, et al. Cytotoxicity of psammaplin A from a two-sponge association may correlate with the inhibition of DNA replication. BMC Cancer. 2004 Sep 30;4:70. [Content Brief]
[8]. Mora FD, et al. Bioassay for the identification of natural product-based activators of peroxisome proliferator-activated receptor-gamma (PPARgamma): the marine sponge metabolite psammaplin A activates PPARgamma and induces apoptosis in human breast tumor cells. J Nat Prod. 2006 Apr;69(4):547-52. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (stored under nitrogen). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 1.5051 mL | 7.5257 mL | 15.0514 mL | 37.6285 mL |
| 5 mM | 0.3010 mL | 1.5051 mL | 3.0103 mL | 7.5257 mL | |
| 10 mM | 0.1505 mL | 0.7526 mL | 1.5051 mL | 3.7629 mL | |
| 15 mM | 0.1003 mL | 0.5017 mL | 1.0034 mL | 2.5086 mL | |
| 20 mM | 0.0753 mL | 0.3763 mL | 0.7526 mL | 1.8814 mL | |
| 25 mM | 0.0602 mL | 0.3010 mL | 0.6021 mL | 1.5051 mL | |
| 30 mM | 0.0502 mL | 0.2509 mL | 0.5017 mL | 1.2543 mL | |
| 40 mM | 0.0376 mL | 0.1881 mL | 0.3763 mL | 0.9407 mL | |
| 50 mM | 0.0301 mL | 0.1505 mL | 0.3010 mL | 0.7526 mL |
Psammaplin A Related Classifications
HY-N2150 Related Classifications
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