2. Metabolic Enzyme/Protease Apoptosis Immunology/Inflammation NF-κB
  3. Carbonic Anhydrase Apoptosis NOD-like Receptor (NLR) Interleukin Related Reactive Oxygen Species (ROS)
  4. CAII-IN-15

CAII-IN-15 is a potent carbonic anhydrase II (CA II) inhibitor with a hCA II IC50 of 10 nM. CAII-IN-15 elevates cGMP levels, releases nitric oxide, reduces oxidative stress, and exhibits neuroprotective activity in vitro. CAII-IN-15 inhibits NLRP3 inflammasome activation, reduces neuronal apoptosis. CAII-IN-15 reduces Intraocular pressure (IOP) in rabbits. CAII-IN-15 can be used for the research of glaucoma.

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CAII-IN-15

CAII-IN-15 Chemical Structure

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CAII-IN-15 Related Antibodies

Top Publications Citing Use of Products

View All Carbonic Anhydrase Isoform Specific Products:

View All Isoforms
CA CA I CA Ⅱ CA IX CA XII CA VII CA VI CA VA CA VB CA XIII CA XIV

View All NOD-like Receptor (NLR) Isoform Specific Products:

View All Isoforms
NLRP3 NLRP1 NOD1 NOD2

View All Interleukin Related Isoform Specific Products:

View All Isoforms
IL-1 IL-2 IL-3 IL-4 IL-5 IL-6 IL-8 IL-10 IL-12 IL-13 IL-15 IL-17 IL-23 IL-7 IL-33 IL-22 IL-18

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Description

CAII-IN-15 is a potent carbonic anhydrase II (CA II) inhibitor with a hCA II IC50 of 10 nM. CAII-IN-15 elevates cGMP levels, releases nitric oxide, reduces oxidative stress, and exhibits neuroprotective activity in vitro. CAII-IN-15 inhibits NLRP3 inflammasome activation, reduces neuronal apoptosis. CAII-IN-15 reduces Intraocular pressure (IOP) in rabbits. CAII-IN-15 can be used for the research of glaucoma[1].

IC50 & Target[1]

hCA II

10 nM (IC50)

hCA IX

32 nM (IC50)

hCA I

430 nM (IC50)

hCA XII

19 nM (IC50)

NLRP3 inflammasome

 

In Vitro

CAII-IN-15 (compound B6) (0.5 nM-5 mM; 15 min) potently and selectively inhibits recombinant human CA II with an IC50 of 10 nM, and demonstrates moderate inhibition of hCA I (IC50 = 430 nM), hCA IX (IC50 = 32 nM), and hCA XII (IC50 = 19 nM)[1].
CAII-IN-15 binds to the active site of CA II via Zn2+ coordination, hydrogen bonding with THR199 and GLN92, and π-π stacking with PHE131, supporting its potent inhibitory activity[1].
CAII-IN-15 (10 μM; 24 h) elevates cGMP levels in human trabecular meshwork (HTM) cells, confirming activation of the NO/sGC/cGMP signaling pathway[1].
CAII-IN-15 (5-20 μM; 4 h) provides concentration-dependent neuroprotection against oxygen-glucose deprivation (OGD)-induced injury in SH-SY5Y cells[1].
CAII-IN-15 (10 μM; 24 h) inhibits LPS (HY-D1056)-induced increase in IL-1β and NLRP3 inflammasome in Müller cells [1].
CAII-IN-15 (10 μM; 4 h) suppresses OGD/R-induced ROS elevation in retinal precursor R28 cells[1].
CAII-IN-15 (0.032-100 μM; 24 h) exhibits dose-dependent cytotoxicity across multiple ocular cell types[1].
CAII-IN-15 (1.56-50.00 μg/mL; 1 h) shows no significant hemolytic activity against rabbit erythrocytes at concentrations from 1.56 μg/mL to 50.00 μg/mL, with hemolysis rates consistently below 5%, demonstrating excellent blood compatibility[1].
CAII-IN-15 (0-30 μM) does not significantly inhibit the hERG potassium channel at concentrations up to 30 μM, indicating a low risk of arrhythmias and favorable cardiac safety[1].

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

CAII-IN-15 Related Antibodies

ELISA Assay[1]

Cell Line: human trabecular meshwork (HTM) cells
Concentration: 10 μM
Incubation Time: 24 h
Result: Significantly Increased intracellular cGMP levels to approximately 15.8 nmol/L.

Cell Viability Assay[1]

Cell Line: SH-SY5Y cells
Concentration: 5; 10; 20 μM
Incubation Time: 4 h
Result: Restored OGD-reduced cell viability to 88.10% (5 μM), 91.12% (10 μM), and 93.71% (20 μM).
Showed concentration-dependent neuroprotection.

ELISA Assay[1]

Cell Line: lipopolysaccharide (LPS)-stimulated Müller cells
Concentration: 10 μM
Incubation Time: 24 h
Result: Substantially reduced LPS-induced ASC speck counts and IL-1β concentrations.

Cell Viability Assay[1]

Cell Line: conjunctival cells, human corneal epithelial cells (HCEC), human trabecular meshwork cells (HTMC), lens B3 cells, retinal R28 cells, and 661W cells
Concentration: 0.032; 0.16; 0.8; 4 μM (conjunctival cells); 0.8; 4; 20; 100 μM (HCEC, HTMC, B3, R28, 661W cells)
Incubation Time: 24 h
Result: Decreased conjunctival cell viability from 97.76% to 76.76% across tested concentrations, with 15.09% higher viability than brinzolamide at 0.032 μM.
Decreased HCEC viability from 99.67% to 76.00%, with 5.33% higher viability than brinzolamide at 100 μM.
Decreased HTMC viability from 99.83% to 91.00%, with 3.73% higher viability than brinzolamide at 4 μM.
Decreased B3 cell viability from 99.67% to 90.33%, with 3.09% higher viability than brinzolamide at 4 μM.
Decreased R28 cell viability from 95.90% to 70.67%, with 7.10% higher viability than brinzolamide at 4 μM.
Decreased 661W cell viability from 91.71% to 75.97%, with 10.86% higher viability than brinzolamide at 4 μM.
In Vivo

CAII-IN-15 (compound B6) (0.05 mL in 1% carbomer suspension; topical (conjunctival sac instillation); single dose; or twice daily for 28 days) demonstrates acute and chronic IOP-lowering efficacy in rabbits[1].
CAII-IN-15 (1% carbomer suspension, 0.1 mL; topical (conjunctival sac instillation); single dose) exhibits minimal ocular irritation in rabbits[1].
CAII-IN-15 (100 μL 1% solution; topical (ocular instillation); single dose) releases nitric oxide in rabbit aqueous humor[1].

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

Animal Model: Male New Zealand white rabbits ( 2-3 months old, 2-2.5 kg) bilateral intravitreally injected with 0.05 mL 5% hypertonic saline[1]
Dosage: 0.05 mL in 1% carbomer suspension
Administration: topical (conjunctival sac instillation); single dose
Result: Achieved a maximum IOP reduction of -6.5 mmHg at 30 minutes post-administration.
Exhibited sustained efficacy lasting until 240 minutes.
Animal Model: Male New Zealand white rabbits ( 2-3 months old, 2-2.5 kg) bilateral intravitreally injected with with 0.1 mL Carbomer (HY-W250721D)[1]
Dosage: 0.05 mL in1% carbomer suspension
Administration: topical (conjunctival sac instillation); twice daily; 28 days
Result: Provided consistent additional IOP reduction throughout the core observation period (days 10-26), with peak differences of 3.0 mmHg recorded on days 14 and 17.
Animal Model: Male New Zealand white rabbits ( 2-3 months old, 2-2.5 kg)[1]
Dosage: 0.1 mL in 1% carbomer suspension
Administration: topical (conjunctival sac instillation); single dose
Result: At 1 hour post-instillation, showed mild conjunctival hyperemia and minimal secretion with a total irritation score of 0.75.
Scores returned to baseline (0) by 2 hours.
Classified as a non-irritant (maximum score ≤1).
Animal Model: Male New Zealand white rabbits ( 2-3 months old, 2-2.5 kg)[1]
Dosage: 1% solution, 100 μL
Administration: topical (ocular instillation); single dose
Result: Released nitric oxide at a concentration of 5.75-6.21 μM at 0.5 hour post-administration.
Decreased Nitric oxide release sharply at 1 hour and 1.5 hours post-administration.
Molecular Weight

351.33

Formula

C14H13N3O6S
SMILES

O=C(NC1=CC=C(S(=O)(N)=O)C=C1)C2=CC=C(CO[N+]([O-])=O)C=C2
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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CAII-IN-15 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:

CAII-IN-15Carbonic AnhydraseApoptosisNOD-like Receptor (NLR)Interleukin RelatedReactive Oxygen Species (ROS)Carbonate dehydrataseILCYP1A2human trabecular meshwork cellsNLRP3 inflammasomeSH-SY5Y cellsMüller cellshuman CA IIrabbit erythrocytesretinal precursor R28 cellscarbonic anhydrase IIhERG potassium channelInhibitorinhibitorinhibit

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