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Dermatan sulphate sodium
CAS No. 54328-33-5
Dermatan sulphate sodium( —— )
Catalog No. M37544 CAS No. 54328-33-5
Dermatan sulphate sodium, a glycosaminoglycan and thrombin inactivator, exhibits antithrombotic activity by selectively catalyzing the inactivation of thrombin via heparin cofactor II, without interaction with antithrombin III.
Purity : >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
| Size | Price / USD | Stock | Quantity |
| 2MG | 137 | Get Quote |
|
| 5MG | 181 | Get Quote |
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| 10MG | 271 | Get Quote |
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| 25MG | 469 | Get Quote |
|
| 50MG | 672 | Get Quote |
|
| 100MG | 972 | Get Quote |
|
| 500MG | Get Quote | Get Quote |
|
| 1G | Get Quote | Get Quote |
|
Biological Information
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Product NameDermatan sulphate sodium
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NoteResearch use only, not for human use.
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Brief DescriptionDermatan sulphate sodium, a glycosaminoglycan and thrombin inactivator, exhibits antithrombotic activity by selectively catalyzing the inactivation of thrombin via heparin cofactor II, without interaction with antithrombin III.
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DescriptionDermatan sulphate sodium is a glycosaminoglycan and thrombin inactivator with antithrombotic activity. Dermatan sulphate sodium selectively catalyzes the inactivation of thrombin by heparin cofactor II and does not interact with antithrombin III. Dermatan sulphate sodium is highly bioavailable and also reduces Bleomycin (HY-108345)-induced pulmonary fibrosis damage.
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In Vitro——
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In Vivo——
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Synonyms——
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PathwayOthers
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TargetOther Targets
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RecptorOthers
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Research Area——
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Indication——
Chemical Information
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CAS Number54328-33-5
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Formula Weight
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Molecular Formula——
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Purity>98% (HPLC)
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Solubility——
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SMILES——
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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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Kuwanon E
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(S,R,S)-AHPC-Me
(S,R,S)-AHPC-Me (VHL ligand 2) is the (S,R,S)-AHPC-based VHL ligand used in the recruitment of the von Hippel-Lindau (VHL) protein. (S,R,S)-AHPC-Me can be used to synthesize ARV-771.
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RMC-6291
RMC-6291 is an orally active, covalent inhibitor of KRAS G12C (ON) that forms a tri-complex within tumor cells between KRAS G12C (ON) and cyclophilin A (CypA), thereby preventing KRAS G12C (ON) from signaling via steric blockade of RAS effector binding and eliciting deep and durable suppression of RAS pathway activity in KRAS G12C tumor models .
