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Cat. No.: HY-N3426

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Kazinol B

Kazinol B, a prenylated flavan with a dimethyl pyrane ring, is an inhibitor of nitric oxide (NO) production. Kazinol B improves insulin sensitivity by enhancing glucose uptake via the insulin-Akt signaling pathway and AMPK activation. Kazinol B has the potential for diabetes mellitus research.

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CAS No.: 99624-27-8
화학식: C₂₅H₂₈O₄
분자량:392.49

보관:

Please store the product under the recommended conditions in the Certificate of Analysis.

Data Sheet (272 KB)

Kazinol B Chemical Structure

CAS No.: 99624-27-8

Amount: USD 0.00

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- 제품 설명
- IC₅₀ & Target
- Cellular Effect
- In Vitro
Chemical Information
Protocol (2)
순도&문서
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

제품 설명

IC₅₀ & Target

^[1]

AMPK

All NO Synthase Isoforms :

All Akt Isoforms :

All AMPK Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
A549	IC₅₀	>100 μM Compound: (-)-4	Cytotoxicity against human A549 cells by MTT assay Cytotoxicity against human A549 cells by MTT assay	[PMID: 28371676]
Hep 3B2	IC₅₀	39 μM Compound: (-)-4	Cytotoxicity against human Hep3B cells by MTT assay Cytotoxicity against human Hep3B cells by MTT assay	[PMID: 28371676]
HepG2	IC₅₀	58.4 μM Compound: (-)-4	Cytotoxicity against human HepG2 cells by MTT assay Cytotoxicity against human HepG2 cells by MTT assay	[PMID: 28371676]
MCF7	IC₅₀	>100 μM Compound: (-)-4	Cytotoxicity against human MCF7 cells by MTT assay Cytotoxicity against human MCF7 cells by MTT assay	[PMID: 28371676]
Platelet	IC₅₀	32.6 μM Compound: 12	Antiplatelet activity against rabbit platelets assessed as arachidonic acid-induced platelet aggregation by turbidimetric method Antiplatelet activity against rabbit platelets assessed as arachidonic acid-induced platelet aggregation by turbidimetric method	[PMID: 8864236]
RAW264.7	IC₅₀	29.31 μM Compound: 168	Antiinflammatory activity against mouse RAW264.7 cells assessed as reduction of LPS-induced NO production Antiinflammatory activity against mouse RAW264.7 cells assessed as reduction of LPS-induced NO production	[PMID: 37683361]

In Vitro

Kazinol B (2, 10 and 20 μM; 72 hours) shows no toxicity to adipocytes in 3T3-L1 cells^[1].
Kazinol B (2-20 μM; 72 hours) dose-dependently increases lipid accumulation by 2.4-fold (at 20 μM) treatment as compared with MDI-treated cells^[1].
Kazinol B (2-20 μM; 5 days) dose-dependently increases PPARγ and C/EBPα protein and mRNA levels in MDI-treated 3T3-L1 adipocytes. Kazinol B increases the mRNA level of adiponectin in a dose-dependent manner^[1].
Kazinol B (2-20 μM; 24 hours) increases the retained 2?NBDG-fluorescence in cells in a dose-dependent manner in differentiated 3T3-L1 adipocytes and C2C12 myoblasts. Kazinol B dependently increases the MDI-stimulated GLUT4 mRNA level up to 4.7-fold as compared with MDI-only treated cells^[1].
Kazinol B (10-20 μM; pre-treated for 1 h followed by 1 h insulin) dose-dependently increases insulin-dependent Akt phosphorylation. Kazinol B alone strongly induces Akt phosphorylation compared with untreated cells. Kazinol B also increased insulin-stimulated AMPK phosphorylation^[1].
Kazinol B (6.25, 12.5, 25, 50 μM; 18 hours) dose-dependently reduces amounts of iNOS protein in macrophages (RAW 264.7 cells) activated by LPS (1 ug/mL)^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.

Chemical Information

CAS No. 99624-27-8
분자량 392.49
화학식 C₂₅H₂₈O₄
SMILES

C/C(C)=C/CC1=C([C@H]2OC3=CC(O)=CC=C3CC2)C=C4C(OC(C)(C)C=C4)=C1O
Structure Classification
- Phenols
- Polyphenols
Initial Source
- Plants
- other families
선적

Room temperature in continental US; may vary elsewhere.
보관

Please store the product under the recommended conditions in the Certificate of Analysis.

Protocol

All Signal Pathway Related

Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked

순도&문서

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (272 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Hyejin Lee, et al. Kazinol B from Broussonetia kazinoki improves insulin sensitivity via Akt and AMPK activation in 3T3-L1 adipocytes. Fitoterapia. 2016 Jul;112:90-6. [Content Brief]

[2]. Jae-Ha Ryu, et al. Fitoterapia. 2003 Jun;74(4):350-4.Inhibition of nitric oxide production on LPS-activated macrophages by kazinol B from Broussonetia kazinoki. [Content Brief]

Calculators

몰농도 계산기

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

농도 희석 계산기

Concentration _(start) × Volume _(start) = Concentration _(final) × Volume _(final)

Concentration _(start) Concentration _(start)

Volume _(start) Volume _(start)

Concentration _(final) Concentration _(final)

Volume _(final) Volume _(final)

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Bioz

Keywords

MOQ

Minimum order quantity

100 mg

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Amount: USD 0.00

Biological Activity
- 제품 설명
- IC₅₀ & Target
- In Vitro
Chemical Information
Protocol
순도&문서
References

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Kazinol B

All NO Synthase Isoforms

All Akt Isoforms

All AMPK Isoforms