2. Apoptosis
  3. RIP kinase Ferroptosis
  4. RIPK1-IN-33

RIPK1-IN-33 is a blood-brain barrier-permeable and orally active RIPK1 inhibitor, with an IC50 of 0.115 μM. RIPK1-IN-33 demonstrates remarkable anti-ferroptosis activity, radical scavenging capacity (IC50 = 123.3 μM), and anti-lipid peroxidation effects (IC50 = 9.72 μM). RIPK1-IN-33 markedly reduces cerebral infarction volume and improves neurological function scores in transient middle cerebral artery occlusion (tMCAO) model. RIPK1-IN-33 can be used for the study of ischemic stroke.

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RIPK1-IN-33 Chemical Structure

RIPK1-IN-33 Chemical Structure

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RIPK1-IN-33 Related Antibodies

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Description

RIPK1-IN-33 is a blood-brain barrier-permeable and orally active RIPK1 inhibitor, with an IC50 of 0.115 μM. RIPK1-IN-33 demonstrates remarkable anti-ferroptosis activity, radical scavenging capacity (IC50 = 123.3 μM), and anti-lipid peroxidation effects (IC50 = 9.72 μM). RIPK1-IN-33 markedly reduces cerebral infarction volume and improves neurological function scores in transient middle cerebral artery occlusion (tMCAO) model. RIPK1-IN-33 can be used for the study of ischemic stroke[1].

In Vitro

RIPK1-IN-33 (Compound 23a) (30-60 min) demonstrates remarkable radical scavenging DAPH capacity (IC50 = 123.3 μM), and antioxidant MDA effects (IC50 = 9.72 μM)[1].
RIPK1-IN-33 (0.0076-50 μM, 17 h) dose-dependently reduces the mRNA expression level of PTGS2 (IC50 = 0.156 μM) in HT-1080 cells[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

RIPK1-IN-33 Related Antibodies

Real Time qPCR[1]

Cell Line: HT-1080 cells
Concentration: 0.0076, 0.0227, 0.0686, 0.206, 0.617, 1.9, 5.6, 16.7, 50 μM
Incubation Time: 17 h
Result: Reduced the mRNA expression level of PTGS2 (IC50 = 0.156 μM) in HT-1080 cells.
Displayed markedly superior anti-ferroptotic activity compared to Edaravone (HY-B0099) (IC50 = 4.92 μM).
In Vivo

RIPK1-IN-33 (Compound 23a) (33 mg/kg (68.8 μmol/kg), i.v., twice doses, 24 h) exerts a protective effect in a rat model of cerebral ischemia-reperfusion injury[1].
RIPK1-IN-33 (Compound 23a) (100-200 mg/kg, i.v., single dose or once daily for 7 days) exhibits no mortality or significant adverse events in a rat model of cerebral ischemia-reperfusion injury[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Adult male Sprague-Dawley rats (200-230 g) subjected to transient middle cerebral artery occlusion (tMCAO)[1]
Dosage: 33 mg/kg (68.8 μmol/kg)
Administration: i.v. for twice doses and the second dose was administered 6 h later
Result: Reduced infarct volume in tMCAO rats compared to the vehicle control.
Improved neurological function in tMCAO rats.
Downregulated MDA level.
Reduced the protein expression of necroptosis-associated caspase-3 in the ischemic penumbra.
Downregulated the protein expression of cyclooxygenase-2 (COX-2, encoded by PTGS2).
Upregulated glutathione peroxidase 4 (GPX4) within the ferroptosis pathway.
Animal Model: Adult male Sprague-Dawley rats (200-230 g) subjected to transient middle cerebral artery occlusion (tMCAO)[1]
Dosage: 100, 200 mg/kg
Administration: i.v. for a single dose or i.v. once daily for 7 days
Result: Showed no abnormalities in body weight, food consumption, organ-to-body weight ratios, blood biochemical parameters, or gross necropsy findings.
Molecular Weight

479.52

Formula

C26H27F2N5O2
SMILES

FC1=CC([C@@H]2CC=NN2C(C3CCN(CC4=CC=CC(N5C(CC(C)=N5)=O)=C4)CC3)=O)=CC(F)=C1
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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RIPK1-IN-33 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

RIPK1-IN-33RIP kinaseFerroptosisReceptor-interacting protein kinasesRIPKRIPK1ischemic stroketMCAOferroptosisInhibitorinhibitorinhibit

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