Heliotridine
Heliotridine ((+)-Heliotridine) is a monoesters-type necine base of pyrrolizidine alkaloid with genotoxic and antibacterial properties. Heliotridine can be isolated from the aerial parts of Heliotropium ellipticum, Heliotropium circinatum and other Heliotropium species (Boraginaceae). Heliotridine shows high tolerance in normal human hepatocytes (EC50 > 400 μM). Mediated by the organic cation transporter OCT1, Heliotridine exhibits in vitro growth inhibition and weak antibacterial activity against Drechslera tetramera. Heliotridine can be used in infection-related studies of specific pathogenic bacteria.
Para uso exclusivo en investigación. No vendemos a pacientes.
- No. CAS: 520-63-8
- Fòrmula: C8H13NO2
- Peso molecular:155.19
-
Almacenamiento:
Please store the product under the recommended conditions in the Certificate of Analysis.
Actividad biológica
Descripciòn
In Vitro
Heliotridine (2 mg; 0.1 g/mL) exhibits in vitro antimicrobial activity against Drechslera tetramera with a 7 mm zone of inhibition, and shows no measurable activity against all other tested bacteria and fungi[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
-
No. CAS 520-63-8
-
Peso molecular 155.19
-
Fòrmula C8H13NO2
-
SMILES
OCC1=CCN2[C@@]1([H])[C@@H](O)CC2
-
Synonyms
(+)-Heliotridine
-
Structure Classification
-
Initial Source
-
Envío
Room temperature in continental US; may vary elsewhere.
-
Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocolo
-
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.
-
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
-
Genotoxicity/Mutagenicity Study
The bacterial reverse mutation assay detects point mutations that restore amino-acid prototrophy in auxotrophic Salmonella typhimurium or Escherichia coli tester strains; after exposure to a test article, mutagenic activity is read out as an increased number of revertant colonies on minimal agar compared with the vehicle control. The assay uses tester strains with different mutation targets so that base-substitution and frameshift mutagens can be detected, and testing is performed with and without exogenous mammalian metabolic activation because some chemicals require biotransformation to become mutagenic.
Pureza y Documentación
Referencias
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)