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Breviscapin
CAS No. 116122-36-2
Breviscapin( —— )
Catalog No. M17848 CAS No. 116122-36-2
Breviscapine is the total flavonoid components (the content of scutellarin > or =85%) extracted from the dried whole plant of Erigeron breviscapus.
Purity : >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
| Size | Price / USD | Stock | Quantity |
| 50MG | 38 | In Stock |
|
| 100MG | 46 | In Stock |
|
| 200MG | Get Quote | In Stock |
|
| 500MG | Get Quote | In Stock |
|
| 1G | Get Quote | In Stock |
|
Biological Information
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Product NameBreviscapin
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NoteResearch use only, not for human use.
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Brief DescriptionBreviscapine is the total flavonoid components (the content of scutellarin > or =85%) extracted from the dried whole plant of Erigeron breviscapus.
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DescriptionBreviscapine is the total flavonoid components (the content of scutellarin > or =85%) extracted from the dried whole plant of Erigeron breviscapus.
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In Vitro——
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In Vivo——
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Synonyms——
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PathwayEndocrinology/Hormones
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TargetRAAS
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RecptorOthers
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Research Area——
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Indication——
Chemical Information
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CAS Number116122-36-2
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Formula Weight908.72
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Molecular FormulaC21H18O11
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Purity>98% (HPLC)
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SolubilityIn Vitro:?DMSO : 100 mg/mL (77.32 mM)
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SMILESc1cc(ccc1c1cc(=O)c2c(c(c(cc2o1)O[C@H]1[C@@H]([C@H]([C@@H]([C@H](O1)C(=O)O)O)O)O)O)O)O
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Chemical Name——
Shipping & Storage Information
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Storage(-20℃)
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ShippingWith Ice Pack
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Stability≥ 2 years
Reference
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Azilsartan Methyl Es...
Azilsartan Methyl Ester is an angiotensin II receptor antagonist. Azilsartan Methyl Ester inhibits specific binding of [125I]AII (0.2 nM) to bovine adrenal cortex with IC50 value is 0.44uM.
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H-Val-Pro-Pro-OH
H-Val-Pro-Pro-OH is an inhibitor of Angiotensin I converting enzyme (ACE)( IC50 : 9 μM).
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N-Acetyl-Ser-Asp-Lys...
Acetyl Ser-Asp-Lys-Pro is formed in bone marrow cells by enzymatic processing of thymosin β4. It inhibits the entry of pluripotent hemopoietic stem cells into S-phase of the cell cycle and protects against Ara-C lethality in mice.N-Acetyl-Ser-Asp-Lys-Pro (AcSDKP) is a specific substrate for the N-terminal site of ACE and increases 5-fold during ACE inhibitor therapy.??AcSDKP inhibited the proliferation of isolated cardiac fibroblasts (P<0.05) but significantly stimulated the proliferation of vascular smooth muscle cells.?
