IDN-7314
IDN-7314 is a pan-Caspase inhibitor with an IC50 of 0.2-7 nM against all tested Caspases. IDN-7314 abrogates Jo2-induced caspase-3/7 activity. IDN-7314 reduces the procoagulant activity of tissue factor in hepatocytes. IDN-7314 is applicable to research related to chemically induced hepatitis, fulminant liver failure and apoptotic liver injury.
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- CAS No.: 254750-11-3
- Formule: C22H17F6N3O7
- Masse moléculaire:549.38
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Activité biologique
Description
IC50 & Target
[1]|
Caspase 3 |
Caspase-7 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| Jurkat | IC50 |
6.3 nM
Compound: 1, IDN-7314
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Antiapoptotic activity against Fas-induced apoptosis in human Jurkat cells
Antiapoptotic activity against Fas-induced apoptosis in human Jurkat cells
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[PMID: 19013793] |
In Vitro
IDN-7314 is a potent pan-caspase inhibitor, with IC50 values of 0.2-7 nM for all tested caspases[1].
IDN-7314 (100 nM) abolishes Jo2-induced caspase-3/7 activity and significantly reduces hepatocyte tissue factor procoagulant activity and release of tissue factor-positive microvesicles[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
IDN-7314 (3 mg/kg; i.p.; single dose) inhibits caspase activation, prevents procoagulant changes, and reduces hepatocellular injury in Mus musculus (mice) with Fas-induced apoptotic liver injury[2]. Wait, no-wait, the original text uses "mice" not the Latin name. Let me correct that to follow the original content strictly:\n\nIDN-7314 (3 mg/kg; i.p.; single dose) inhibits caspase activation, prevents procoagulant changes, and reduces hepatocellular injury in mice with Fas-induced apoptotic liver injury[2].\n\nWait, rechecking: "Fas" is an English target name, so it should be bold. Citations get superscript. No other entities here-no Latin species name used (the text says "mice" not the Latin binomial, so we don't alter that), no gene symbols, chemical formulas, etc. That's correct.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley (female, 150-200 g, chemical-induced hepatitis model)[1]
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Dosage:10 mg/kg (6-hour observation group); 10 mg/kg (24-hour two-dose group); 10 mg/kg (24-hour pretreatment group)
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Administration:i.p.; two doses at 3 and 4.5 hours post-galactosamine (6-hour group); two doses at 3 and 6 hours post-galactosamine (24-hour two-dose group); three doses 30 minutes pre-galactosamine, 3 and 6 hours post-galactosamine (24-hour pretreatment group)
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Result:Reduced the percentage of apoptotic hepatocytes by 76% (from 5.0 ± 0.34% to baseline-like levels) at 6 hours post-galactosamine.
Reduced hepatic and plasma caspase-3 activities to control levels at 6 hours post-galactosamine.
Prevented procaspase-3 processing to its active fragment at 6 hours post-galactosamine.
Did not reduce plasma ALT activities at 6 hours post-galactosamine.
Had no significant effect on oncotic cell counts at 6 hours post-galactosamine.
Reduced plasma ALT levels by 57% (p < 0.05) at 24 hours post-galactosamine (two-dose schedule).
Reduced hepatocellular oncosis by 24% (p > 0.05) at 24 hours post-galactosamine (two-dose schedule).
Reduced hepatic and plasma caspase-3 activities to baseline at 24 hours post-galactosamine (two-dose schedule).
Reduced the percentage of apoptotic hepatocytes by 71% (from 7.3 ± 1.1% to 2.1 ± 0.4%) at 24 hours post-galactosamine (three-dose pretreatment schedule).
Had no significant effect on plasma ALT activities or oncotic cell counts at 24 hours post-galactosamine (three-dose pretreatment schedule).
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Animal Model:Sprague-Dawley (female, 150-200 g, chemical-induced hepatitis model)[1]
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Dosage:10 mg/kg
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Administration:i.p.; two doses at 3 and 4.5 hours post-galactosamine/endotoxin injection
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Result:Reduced hepatic caspase-3 activities from 194 ± 33 ΔF/min/mg protein to baseline 16 ± 5 ΔF/min/mg protein.
Reduced plasma caspase-3 activities from 12.9 ± 1.5 ΔF/min/mg protein to baseline 0.2 ± 0.2 ΔF/min/mg protein.
Reduced the percentage of apoptotic hepatocytes by 80% (from 7.33 ± 0.32% to 1.50 ± 0.29%).
Reduced plasma ALT activities by 50% (from 708 ± 54 IU/L to 359 ± 34 IU/L).
Reduced the percentage of oncotic hepatocytes by 33% (from 2.35 ± 0.22% to 1.58 ± 0.13%).
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Animal Model:C57BL/6J (male, 8-12 weeks old, Fas-induced apoptotic liver injury model)[2]
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Dosage:3 mg/kg
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Administration:i.p.; single dose (administered 1 hour after Jo2 injection)
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Result:Attenuated Jo2-induced hepatic cleaved caspase-3 levels.
Abolished Jo2-induced increases in plasma alanine aminotransferase (ALT) activity.
Eliminated Jo2-induced hepatic sinusoidal congestion/hemorrhage.
Completely prevented Jo2-induced increases in plasma TF-positive microvesicle levels.
Blocked Jo2-induced increases in plasma thrombin-antithrombin (TAT) levels.
Attenuated Jo2-induced hepatic fibrin(ogen) β chain accumulation.
Abolished Jo2-induced hepatic cleaved caspase-3 staining and dramatically reduced hepatic fibrin(ogen) deposition.
Chemical Information
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CAS No. 254750-11-3
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Masse moléculaire 549.38
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Formule C22H17F6N3O7
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SMILES
O(CC([C@@H](NC([C@@H](NC(C(NC1=C(F)C=CC=C1F)=O)=O)C)=O)CC(O)=O)=O)C2=C(F)C(F)=CC(F)=C2F
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
Pureté et documentation
Références
[1]. Gujral JS, et al. Oncotic necrosis and caspase-dependent apoptosis during galactosamine-induced liver injury in rats. Toxicol Appl Pharmacol. 2003;190(1):37-46. [Content Brief]
[2]. Kopec AK, et al. Caspase Inhibition Reduces Hepatic Tissue Factor-Driven Coagulation In Vitro and In Vivo. Toxicol Sci. 2018;162(2):396-405. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
IDN-7314 Related Classifications
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