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SR 11302
CAS No. 160162-42-5
SR 11302( —— )
Catalog No. M27717 CAS No. 160162-42-5
SR 11302 is an inhibitor of activator protein-1 (AP-1).
Purity : >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
| Size | Price / USD | Stock | Quantity |
| 5MG | 115 | Get Quote |
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| 10MG | 178 | Get Quote |
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| 25MG | 357 | Get Quote |
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| 50MG | 557 | Get Quote |
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| 100MG | 795 | Get Quote |
|
| 200MG | Get Quote | Get Quote |
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| 500MG | Get Quote | Get Quote |
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| 1G | Get Quote | Get Quote |
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Biological Information
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Product NameSR 11302
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NoteResearch use only, not for human use.
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Brief DescriptionSR 11302 is an inhibitor of activator protein-1 (AP-1).
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DescriptionSR 11302 is an inhibitor of activator protein-1 (AP-1).(In Vitro):SR 11302 can inhibit the growth of breast cancer cell line T-47D, the lung cancer line Calu-6, and HeLa cells. SR 11302 had very little effect on either the proliferation or the differentiation of HL-60, fresh APL, and NB4 cells.(In Vivo):In an AP-1-luciferase transgenic mouse carcinogenesis model, SR11302 significantly inhibits both AP-1 activations in 7,12-dimethyl benz(a)anthracene-initiated mouse skin and 12-O-tetradecanoylphorbol-13-acetate-induced papilloma formation.
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In VitroSR 11302 (SR11302) show strong anti-AP-1 activity with selective binding with RARα and RARγ, but not with RARβ and RXRα. SR 11302 (SR-11302; 1 μM) inhibits AP-1 transcription factor activity and decreases aldosterone levels by 61.9% in hypoxia-treated cells. SR 11302 (SR-11302; 2 μM; 48 hours) inhibits Helicobacter pylori (H. pylori)-induced cell proliferation in adenocarcinoma gastric (AGS) cells.SR 11302 (2 μM; 24 hours) inhibits H. pylori-induced expression of β-catenin and c-myc in AGS cells.
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In VivoSR 11302 (SR11302; low dose 0.5 mg/kg and high dose 1 mg/kg body weight; orally gavaged daily) treatment reduces the total vascular lesion number and lesion size in Vldlr-/- mice in a dose-dependent manner. Animal Model:Vldlr-/- mice Dosage:Low dose 0.5 mg/kg and high dose 1 mg/kg body weight Administration:Orally gavaged daily from P5 to P15 Result:High-dose from P5 to P15 reduced the total vascular lesion number by 48% and decreased the lesion size by 40%, without detectable signs of toxicity in mice, including no change in body weight.
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Synonyms——
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PathwayCell Cycle/DNA Damage
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TargetDNA/RNA Synthesis
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Recptor11β-HSD1|Gap Junction Protein
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Research Area——
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Indication——
Chemical Information
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CAS Number160162-42-5
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Formula Weight376.54
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Molecular FormulaC26H32O2
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Purity>98% (HPLC)
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SolubilityIn Vitro:?DMSO : 25 mg/mL (66.40 mM)
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SMILESCC(C=CC=C(C=CC1=C(C)CCCC1(C)C)c1ccc(C)cc1)=CC(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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NSAH?
NSAH is a nonnucleoside inhibitor of human ribonucleotide reductase (hRR).with cell-free IC50 of 32 μM and cell-based IC50 of ~250 nM, respectively.A unique nonnucleoside small-molecule hRR inhibitor, naphthyl salicylic acyl hydrazone (NSAH), using virtual screening, binding affinity, inhibition, and cell toxicity assays.?NSAH binds to hRRM1 with an apparent dissociation constant of 37 μM, and steady-state kinetics reveal a competitive mode of inhibition.?
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JH-RE-06
JH-RE-06 disrupts mutagenic translesion synthesis (TLS) by preventing the recruitment of mutagenic POLζ. JH-RE-06 is an effective REV1-REV7 interface inhibitor (IC50=0.78 μM; Kd=0.42 μM), which targets REV1 that interacts with the REV7 subunit of POLζ. JH-RE-06 also improves chemotherapy.
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Loureirin B
Loureirin B can downregulate the expression of fibrosis-related molecules by regulating MMPs and TIMPs levels, inhibit scar fibroblast proliferation and suppress TGF-β1-induced fibrosis, during which TGF-β1/Smad2/3 pathway is likely involved.
