STIM1-TFR1-IN-1
STIM1-TFR1-IN-1 is an orally active stromal interaction molecule 1 (STIM1)-transferrin receptor 1 (TFR1) protein complex inhibitor with a Kd of 2.18 μM for STIM1-CD protein. STIM1-TFR1-IN-1 blocks STIM1-TFR1 interaction and reduce TFR1-mediated iron uptake activity. STIM1-TFR1-IN-1 inhibits ferroptosis, lipid peroxidation and ROS production, enhances glutathione peroxidase 4 (GPX4) activity and glutathione/oxidized glutathione ratio, and rescues ferroptosis-associated mitochondrial morphological changes. STIM1-TFR1-IN-1 exhibits neuroprotective
effects and reduces brain injury. STIM1-TFR1-IN-1 can be used for the research of intracerebral hemorrhage.
For research use only. We do not sell to patients.
- CAS No.: 2196106-61-1
- Formula: C15H21N5OS
- Molecular Weight:319.43
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
effects and reduces brain injury. STIM1-TFR1-IN-1 can be used for the research of intracerebral hemorrhage[1].
IC50 & Target
[1]|
TFR1 |
GPX4 |
In Vitro
STIM1-TFR1-IN-1 (Compound S-IN-1) (0.15625-5 μM) directly and specifically binds to the STIM1-CD protein with a Kd of 2.18 μM[1].
S-IN-1 (10-20 μM) inhibits the interaction between STIM1 and TFR1 in HT22 mouse neuronal cells exposed to Hemin (HY-19424) to model ICH[1].
S-IN-1 (0-40 μM) attenuates neuronal ferroptosis and increases the vitality of neuronal cells in Hemin-treated HT22 mouse neuronal cells by reducing iron accumulation, lipid peroxidation, and ROS, while enhancing antioxidant defense system[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J (adult male, 10-week-old, 20-25 g, intracerebral hemorrhage induced by autologous blood injection)[1]
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Dosage:10 mg/kg
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Administration:p.o.; once every 24 h
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Result:Reduced brain edema, increased the number of surviving neurons, and lowered plasma neuron-specific enolase (NSE) levels on day 3 post-ICH.
Significantly improved modified neurological severity score (mNSS), corner test scores, cylinder test scores, adhesive removal time, and rotarod fall latency on day 3 post-ICH.
Continuously improved mNSS, corner test scores, cylinder test scores, adhesive removal time, rotarod fall latency, novel object location (NOL) discrimination ratios, and novel object recognition (NOR) discrimination ratios over 14 days post-ICH compared to vehicle controls.
Chemical Information
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CAS No. 2196106-61-1
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Molecular Weight 319.43
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Formula C15H21N5OS
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SMILES
O=C(NC1=NN=C(C2CCC2)N1)[C@@H](N3C=CC=C3)CCSC
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Immunoprecipitation
Immunoprecipitation (IP) is an experimental method that uses the principle of antibody specific binding to purify and enrich target proteins.
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Ferroptosis Solutions
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death characterized by lethal lipid peroxidation and sensitivity to suppression by iron chelators or lipophilic radical-trapping antioxidants. The core pathway links cystine uptake through system Xc−, glutathione availability, GPX4-dependent detoxification of phospholipid hydroperoxides, iron-dependent oxidative reactions, and polyunsaturated-phospholipid metabolism into a cell-death program that is biochemically and morphologically distinct from apoptosis, necrosis, and autophagy. The ferroptosis pathway is experimentally linked to phenotype through chemical and genetic perturbation. Erastin induces ferroptosis by inhibiting cystine uptake through system Xc− and weakening antioxidant defenses, while GPX4 inhibition or depletion causes lipid peroxide accumulation and ferroptotic cancer-cell death. ACSL4 and oxidizable arachidonoyl- or adrenoyl-containing phosphatidylethanolamines shape ferroptosis sensitivity by con
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Co-Immunoprecipitation
Co-immunoprecipitation technology can verify protein interaction based on the specific immune reaction between antibodies and antigens.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Keywords
- STIM1-TFR1-IN-1
- 2196106-61-1
- Transferrin Receptor
- Ferroptosis
- Reactive Oxygen Species (ROS)
- Glutathione Peroxidase
- STIM1-TFR1 protein complex
- reactive oxygen species
- ferroptosis
- glutathione peroxidase 4
- STIM1
- iron uptake activity
- Lys385 site
- lipid peroxidation
- neuronal iron accumulation
- TFR1
- Inhibitor
- inhibitor
- inhibit