Picrasidine I

CAS# 100234-59-1

Picrasidine I

2D Structure

Catalog No. BCN5819----Order now to get a substantial discount!

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Quality Control of Picrasidine I

3D structure

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Picrasidine I

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Chemical Properties of Picrasidine I

Cas No. 100234-59-1 SDF Download SDF
PubChem ID 5324360 Appearance Yellow powder
Formula C14H12N2O2 M.Wt 240.3
Type of Compound Alkaloids Storage Desiccate at -20°C
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Chemical Name 1-ethenyl-4-methoxy-9H-pyrido[3,4-b]indol-8-ol
SMILES COC1=CN=C(C2=C1C3=C(N2)C(=CC=C3)O)C=C
Standard InChIKey JOHWQLSNGRWJRK-UHFFFAOYSA-N
Standard InChI InChI=1S/C14H12N2O2/c1-3-9-14-12(11(18-2)7-15-9)8-5-4-6-10(17)13(8)16-14/h3-7,16-17H,1H2,2H3
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Picrasidine I

The bark of Picrasma quassioides.

Biological Activity of Picrasidine I

DescriptionPicrasidine I has antiosteoclastogenic effect by inhibiting inflammation induced activation of MAPKs, NF-κB and ROS generation followed by suppressing the gene expression of c-Fos and NFATc1 in osteoclast precursors.
TargetsMAPK | NF-κB | ROS | c-Fos | NFATc1

Protocol of Picrasidine I

Cell Research

Picrasidine I from Picrasma Quassioides Suppresses Osteoclastogenesis via Inhibition of RANKL Induced Signaling Pathways and Attenuation of ROS Production.[Reference: WebLink]

Cellular Physiology & Biochemistry, 2017:1425-1435.

Osteoporosis is a metabolic bone disorder that tortures about millions of people worldwide. Recent study demonstrated agents derived from picrasma quassioides is a promising drug for targets multiple signaling pathways. However its potential in treatment of bone loss has not been fully understood.
METHODS AND RESULTS:
The bone marrow macrophages (BMMs) were cultured and induced with M-CSF and RANKL followed by Picrasidine I (PI) treatment. Then the effects of PI on osteoclast formation were evaluated by counting tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells. Moreover, effects of PI on bone resorption activity of mature osteoclast were studied through bone resorption pit counting and actin ring structure analysis. Further, the involved potential signaling pathways cross-talking were investigated by performed Western blotting and quantitative real-time PCR examination. Results demonstrated PI strongly inhibited RANKL induced osteoclast formation from its precursors. Mechanistically, the inhibitory effect of PI on osteoclast differentiation was due to the suppression of osteoclastogenic transcription factors, c-Fos and NFATc1. Moreover, PI markedly blocked the RANKL-induced osteoclastogenesis by attenuating MAPKs and NF-κB signaling pathways. In addition, PI decreased the ROS generation in osteoclast and osteoblast.
CONCLUSIONS:
Taken together our data demonstrate that PI has antiosteoclastogenic effect by inhibiting inflammation induced activation of MAPKs, NF-κB and ROS generation followed by suppressing the gene expression of c-Fos and NFATc1 in osteoclast precursors.

Picrasidine I Dilution Calculator

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Picrasidine I Molarity Calculator

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Preparing Stock Solutions of Picrasidine I

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 4.1615 mL 20.8073 mL 41.6146 mL 83.2293 mL 104.0366 mL
5 mM 0.8323 mL 4.1615 mL 8.3229 mL 16.6459 mL 20.8073 mL
10 mM 0.4161 mL 2.0807 mL 4.1615 mL 8.3229 mL 10.4037 mL
50 mM 0.0832 mL 0.4161 mL 0.8323 mL 1.6646 mL 2.0807 mL
100 mM 0.0416 mL 0.2081 mL 0.4161 mL 0.8323 mL 1.0404 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on Picrasidine I

Picrasidine I from Picrasma Quassioides Suppresses Osteoclastogenesis via Inhibition of RANKL Induced Signaling Pathways and Attenuation of ROS Production.[Pubmed:29017159]

Cell Physiol Biochem. 2017;43(4):1425-1435.

BACKGROUND/AIMS: Osteoporosis is a metabolic bone disorder that tortures about millions of people worldwide. Recent study demonstrated agents derived from picrasma quassioides is a promising drug for targets multiple signaling pathways. However its potential in treatment of bone loss has not been fully understood. METHODS: The bone marrow macrophages (BMMs) were cultured and induced with M-CSF and RANKL followed by Picrasidine I (PI) treatment. Then the effects of PI on osteoclast formation were evaluated by counting tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells. Moreover, effects of PI on bone resorption activity of mature osteoclast were studied through bone resorption pit counting and actin ring structure analysis. Further, the involved potential signaling pathways cross-talking were investigated by performed Western blotting and quantitative real-time PCR examination. RESULTS: Results demonstrated PI strongly inhibited RANKL induced osteoclast formation from its precursors. Mechanistically, the inhibitory effect of PI on osteoclast differentiation was due to the suppression of osteoclastogenic transcription factors, c-Fos and NFATc1. Moreover, PI markedly blocked the RANKL-induced osteoclastogenesis by attenuating MAPKs and NF-kappaB signaling pathways. In addition, PI decreased the ROS generation in osteoclast and osteoblast. CONCLUSION: Taken together our data demonstrate that PI has antiosteoclastogenic effect by inhibiting inflammation induced activation of MAPKs, NF-kappaB and ROS generation followed by suppressing the gene expression of c-Fos and NFATc1 in osteoclast precursors.

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