NOD-IN-1 1 mg | 99.43%
TargetMol
NOD-IN-1 is a potent mixed inhibitor of nucleotide-binding oligomerization domain (NOD)-like receptors.
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NOD-IN-1 10 mg | 99.43%
TargetMol
NOD-IN-1 is a potent mixed inhibitor of nucleotide-binding oligomerization domain (NOD)-like receptors.
More Information Supplier PageNOD-IN-1
Macozinone 5 mg | 100.00%
TargetMol
Macozinone (PBTZ169) inhibits decaprenylphosphoryl-β-d-ribose 2′-oxidase (DprE1), more efficiently than BTZ043.
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Macozinone 50 mg | 100.00%
TargetMol
Macozinone (PBTZ169) inhibits decaprenylphosphoryl-β-d-ribose 2′-oxidase (DprE1), more efficiently than BTZ043.
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Macozinone 25 mg | 100.00%
TargetMol
Macozinone (PBTZ169) inhibits decaprenylphosphoryl-β-d-ribose 2′-oxidase (DprE1), more efficiently than BTZ043.
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NSC23005 Sodium 100 mg | Purity Not Available
TargetMol
NSC23005 sodium is a novel and effective p18 inhibitor (ED50=5.21 nM) in promoting Hematopoietic stem cells (HSCs) expansion in both murine and human models.
More Information Supplier PageNSC23005 Sodium 10 mg | Purity Not Available
TargetMol
NSC23005 sodium is a novel and effective p18 inhibitor (ED50=5.21 nM) in promoting Hematopoietic stem cells (HSCs) expansion in both murine and human models.
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U93631 5 mg | Purity Not Available
TargetMol
GABAA receptor antagonist that binds the picrotoxin site and stabilizes the inactive form of the channel via allosteric interaction. Accelerates the decay of GABA-induced Cl- currents with little effect on peak amplitude. Also inhibits 5-HT3A receptors via a similar mechanism.
More Information Supplier PageU93631
U93631 50 mg | Purity Not Available
TargetMol
GABAA receptor antagonist that binds the picrotoxin site and stabilizes the inactive form of the channel via allosteric interaction. Accelerates the decay of GABA-induced Cl- currents with little effect on peak amplitude. Also inhibits 5-HT3A receptors via a similar mechanism.
More Information Supplier PageU93631
U93631 25 mg | Purity Not Available
TargetMol
GABAA receptor antagonist that binds the picrotoxin site and stabilizes the inactive form of the channel via allosteric interaction. Accelerates the decay of GABA-induced Cl- currents with little effect on peak amplitude. Also inhibits 5-HT3A receptors via a similar mechanism.
More Information Supplier PageU93631