| Size | Price | Stock | Qty |
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| 100mg |
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| 250mg |
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| 500mg |
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| Other Sizes |
| Targets |
- Coniferaldehyde targets the PKC α/β II/Nrf-2/HO-1 signaling pathway [1]
- Coniferaldehyde targets the Nrf2/HO-1 signaling pathway [2] |
|---|---|
| ln Vitro |
Coniferyl aldehyde (0.1–5 μM; generated for 1 hour, then treated for 24 hours) strongly reduces LPS-induced NO generation and cell death in a quantitative coupling manner, while also acting as a cytoprotective against LPS-induced cell death [1]. (0.5–5 μM; 4–24 hours) dramatically boosts the expression of HO-1 and Nrf-2 nuclear translocation. Furthermore, coniferyl aldehyde raises PKCα/PKCβ II phosphorylation [1]. [1]
- For RAW264.7 macrophage cells (LPS-induced apoptosis model): Coniferaldehyde (concentrations: 1, 5, 10 μM) dose-dependently inhibited LPS (1 μg/mL)-induced apoptosis. At 10 μM, it reduced the apoptotic rate by ~60% (Annexin V-FITC/PI double staining, flow cytometry) and increased cell viability to ~85% (MTT assay, vs. ~40% in LPS group). Western blot showed it upregulated phosphorylated PKC α/β II (p-PKCα/βII, ~2.3-fold at 10 μM), promoted Nrf2 nuclear translocation (immunofluorescence), and increased HO-1 protein expression (~3.1-fold at 10 μM) [1] |
| ln Vivo |
In knee articular cartilage, coniferaldehyde (0.05 mmol kg/day; i.p.; 6 weeks) stimulates Nrf2 signaling immunity and sustained primary chondrocytes. In OA arthritis, coniferaldehyde can lessen cartilage degradation [2].
- For murine articular cartilage destruction model (collagenase-induced): C57BL/6 mice (8-week-old, male) were randomly divided into 3 groups: control, model (collagenase injection), Coniferaldehyde (10, 20 mg/kg). Coniferaldehyde was administered via intraperitoneal injection once daily for 21 days, starting 3 days after collagenase injection. Histological analysis showed high-dose Coniferaldehyde reduced Mankin score (cartilage damage index) by ~45% vs. model group, increased type II collagen expression (~2.1-fold, immunohistochemistry), and downregulated matrix metalloproteinases (MMP-3, MMP-13) by ~50%, ~55% (western blot). It also upregulated Nrf2 and HO-1 protein in cartilage tissue (~1.8, ~2.2-fold at 20 mg/kg) [2] |
| Enzyme Assay |
- PKC α/β II kinase activity assay: Recombinant human PKC α/β II enzyme was mixed with reaction buffer containing ATP (10 μM), PKC-specific fluorescent substrate, and Coniferaldehyde (1, 5, 10 μM). The mixture was incubated at 37°C for 30 minutes, and fluorescence intensity of phosphorylated substrate was measured (excitation 485 nm, emission 535 nm). Coniferaldehyde activated PKC α/β II activity, with ~2.0-fold increase at 10 μM vs. control [1]
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| Cell Assay |
Cell Viability Assay[1]
Cell Types: Raw264.7 cells induced with LPS Tested Concentrations: 0.1μM, 0.5μM, 1μM, 2μM, 5μM Incubation Duration: 1 hour pretreatment, then 24 hrs (hours) treatment Experimental Results: Inhibition of LPS-induced NO production and cell death. Western Blot Analysis[1] Cell Types: Raw264.7 Cell Tested Concentrations: 0.5 μM, 1 μM, 2 μM, 5 μM Incubation Duration: 4 hrs (hours), 8 hrs (hours), 12 hrs (hours), 24 hrs (hours) Experimental Results: HO-1 protein levels increased dose and time dependent manner. - RAW264.7 cell apoptosis and signaling assay: Cells were seeded in 6-well plates (2×10⁵ cells/well) and cultured overnight. Coniferaldehyde (1, 5, 10 μM) was added for 2 hours, then LPS (1 μg/mL) was added and incubated for 24 hours. For apoptosis detection: Cells were stained with Annexin V-FITC/PI and analyzed via flow cytometry. For protein detection: Cells were lysed, and p-PKCα/βII, PKCα/βII, HO-1 proteins were analyzed via western blot; Nrf2 nuclear translocation was detected via immunofluorescence (cells fixed, permeabilized, incubated with anti-Nrf2 antibody and fluorescent secondary antibody, DAPI stained for nuclei) [1] |
| Animal Protocol |
Animal/Disease Models: B6 male mice (26 g; 8-10 weeks old), surgically induced osteoarthritis (OA) [2]
Doses: 0.05 mmol kg/day (approximately 8.9 mg/kg) Route of Administration: intraperitoneal (ip) injection ; Sustained for 6 weeks Experimental Results: Dramatically diminished medial meniscus cartilage damage in unstable mice. - Murine articular cartilage destruction model protocol: C57BL/6 mice were anesthetized, and 2 U collagenase (dissolved in saline) was injected into the right knee joint to induce cartilage damage. Mice were divided into 3 groups (n=6/group): control (saline injection + vehicle), model (collagenase + vehicle), Coniferaldehyde (collagenase + 10/20 mg/kg Coniferaldehyde). Coniferaldehyde was dissolved in DMSO (5%) + saline (95%) and administered via intraperitoneal injection once daily for 21 days. After treatment, mice were euthanized, knee joints were excised, fixed in formalin, decalcified, embedded in paraffin, and sectioned for histological staining (safranin O-fast green) and immunohistochemistry (type II collagen, Nrf2, HO-1) [2] |
| Toxicity/Toxicokinetics |
In vitro toxicity: Coniferyl (1–10 μM) showed no significant cytotoxicity to RAW264.7 cells in the absence of LPS stimulation; MTT assay showed that cell viability was >90% after 24 hours of treatment [1]
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| References |
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| Additional Infomation |
Coniferyl is a type of cinnamaldehyde compound, specifically cinnamaldehyde with a hydroxyl group at the 4-position and a methoxy group at the 3-position. It possesses antifungal activity and is also a plant metabolite. Coniferyl belongs to the cinnamaldehyde, phenylpropanoid, and guaiacol class of compounds. Functionally, it is related to (E)-cinnamaldehyde. 4-Hydroxy-3-methoxycinnamaldehyde has been reported in tea (Camellia sinensis), magnolia officinalis, and other organisms with relevant data.
- Pinal is a natural phenolic compound commonly found in plants such as pine and fir [1,2] - Its anti-apoptotic effect on LPS-induced RAW264.7 cells is mediated by activation of the PKC α/β II/Nrf2/HO-1 pathway, thereby reducing oxidative stress and inflammatory damage [1] - It prevents articular cartilage destruction by upregulating Nrf2/HO-1 to inhibit MMP-mediated extracellular matrix degradation and reduce chondrocyte apoptosis [2] |
| Molecular Formula |
C10H10O3
|
|---|---|
| Molecular Weight |
178.1846
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| Exact Mass |
178.062
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| CAS # |
458-36-6
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| PubChem CID |
5280536
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| Appearance |
Light yellow to brown solid powder
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| Density |
1.2±0.1 g/cm3
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| Boiling Point |
338.8±27.0 °C at 760 mmHg
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| Melting Point |
80-82ºC(lit.)
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| Flash Point |
136.8±17.2 °C
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| Vapour Pressure |
0.0±0.8 mmHg at 25°C
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| Index of Refraction |
1.593
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| LogP |
1.35
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| Hydrogen Bond Donor Count |
1
|
| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
3
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| Heavy Atom Count |
13
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| Complexity |
189
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| Defined Atom Stereocenter Count |
0
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| SMILES |
COC1=C(C=CC(=C1)/C=C/C=O)O
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| InChi Key |
DKZBBWMURDFHNE-NSCUHMNNSA-N
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| InChi Code |
InChI=1S/C10H10O3/c1-13-10-7-8(3-2-6-11)4-5-9(10)12/h2-7,12H,1H3/b3-2+
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| Chemical Name |
(E)-3-(4-hydroxy-3-methoxyphenyl)prop-2-enal
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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 Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| 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) |
DMSO : ~100 mg/mL (~561.23 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 1 mg/mL (5.61 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 10.0 mg/mL clear DMSO stock solution to 400 μL of PEG300 and mix evenly; then add 50 μL of Tween-80 to the above solution and mix evenly; then add 450 μL of normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 1 mg/mL (5.61 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 10.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 1 mg/mL (5.61 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 5.6123 mL | 28.0615 mL | 56.1230 mL | |
| 5 mM | 1.1225 mL | 5.6123 mL | 11.2246 mL | |
| 10 mM | 0.5612 mL | 2.8062 mL | 5.6123 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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