4-Isopropyl-1-methylcyclohexanol
4-Isopropyl-1-methylcyclohexanol is a terpenoid component. 4-Isopropyl-1-methylcyclohexanol can be isolated from extracts of peppermint (Mentha × piperita). 4-Isopropyl-1-methylcyclohexanol reduces the level of mitotic nuclei, exhibits no antibacterial activity against bacteria, and shows no antiviral activity against respiratory syncytial virus.
For research use only. We do not sell to patients.
- CAS No.: 21129-27-1
- Formula: C10H20O
- Molecular Weight:156.27
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
4-Isopropyl-1-methylcyclohexanol (5.01 mM; 24 h) reduces mitotic nuclei levels in HEp-2 cancer cells at the 5.01 mM concentration present in peppermint extract, without inducing apoptosis or cytoskeletal disruption[1].
4-Isopropyl-1-methylcyclohexanol (0.05-5 mM; 3 h) does not inhibit the growth of E. coli or S. aureus at concentrations ranging from 0.05 mM to 5 mM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
-
Cell Line:HEp-2 (HeLa-derived) cancer cells
-
Concentration:5.01 mM
-
Incubation Time:24 h
-
Result:Triggered a significant reduction in the amount of detected mitotic nuclei relative to the DMSO control.
Showed no significant changes in apoptotic nuclei or cytoskeletal structure compared to the DMSO control.
Chemical Information
-
CAS No. 21129-27-1
-
Molecular Weight 156.27
-
Formula C10H20O
-
SMILES
OC1(C)CCC(CC1)C(C)C
-
Structure Classification
-
Initial Source
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
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
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)