Hydrochlorides
Medchemexpress LLC 1-(4,4-diphenyl-3-butenyl)-3-piperidinecarboxylic acid hydrochloride | 85375-15-1 | MFCD01321071 | >98.0% | 371.91 | C22H26ClNO2 | 10 MG
Selective GABA transporter 1 (GAT-1) inhibitor supplied as the hydrochloride salt for neuroscience research. It blocks GABA reuptake, is brain-penetrant, and is commonly used to probe GABAergic signaling and transporter pharmacology in vitro and in vivo.
- Selective GAT-1 inhibitor that blocks GABA reuptake.
- Brain-penetrant, suitable for in vivo studies.
- High purity (≥98% by HPLC) for reliable experimental results.
- Hydrochloride salt form for improved solubility in biological assays.
- Available as solid and as solution formats for flexible use.
- Commonly used to study GABA uptake and transporter pharmacology.
Medchemexpress LLC 5,7-Dimethoxy-3-(4-pyridinyl)quinoline dihydrochloride | 1123491-15-5 | 99.1% | 339.22 | 10 MG
DMPQ dihydrochloride is a potent and selective inhibitor of human platelet-derived growth factor receptor β (PDGFRβ) with an IC50 of 80 nM. It is for research use only and not sold to patients.
- Potent and selective inhibitor of human PDGFRβ.
Medchemexpress LLC 5,7-dimethoxy-3-pyridin-4-ylquinoline;dihydrochloride | 1123491-15-5 | MFCD02262123 | 99.1% | 339.22 | 1 MG
DMPQ dihydrochloride is a potent and selective inhibitor of human platelet-derived growth factor receptor β (PDGFRβ) with an IC50 of 80 nM. It is for research use only and not sold to patients.
- Potent and selective inhibitor of human platelet-derived growth factor receptor β (PDGFRβ)
- Inhibits PDGFRβ with an IC50 of 80 nM, useful for research applications.
Medchemexpress LLC 5,7-dimethoxy-3-(4-pyridinyl)quinoline dihydrochloride | 1123491-15-5 | MFCD02262123 | 99.1% | 339.22 g/mol | C16H16Cl2N2O2 | 5 MG
DMPQ dihydrochloride is the dihydrochloride salt of 5,7-dimethoxy-3-(4-pyridinyl)quinoline. It is a small-molecule inhibitor that selectively targets human platelet-derived growth factor receptor β (PDGFRβ) with reported biochemical potency, and is supplied as a light yellow to yellow solid for research use in biochemical and cell-based assays.
- Potent PDGFRβ inhibition with reported IC50 of 80 nM.
- High reported purity suitable for biochemical assays.
- Solid form, convenient for weighing and formulation.
- Available in multiple small pack sizes for research applications.
Medchemexpress LLC AZD5582 dihydrochloride | 1883545-51-4 | 99.9% | 1088.21 | 25 MG
AZD5582 dihydrochloride is an antagonist of the inhibitor of apoptosis proteins (IAPs). It binds to the BIR3 domains of cIAP1, cIAP2, and XIAP with IC50s of 15, 21, and 15 nM, respectively, and induces apoptosis.
- Antagonist of inhibitor of apoptosis proteins (IAPs)
- Binds to BIR3 domains of cIAP1, cIAP2, and XIAP
- Induces apoptosis
- Inhibits cell viability in H1975 NSCLC cells in cooperation with IFNγ or viral double-stranded RNA (dsRNA)
- Downregulates cIAP-1, activates RIPK1, and triggers activation of extrinsic and intrinsic apoptosis pathways in H1975 NSCLC cells
- Involves in apoptosis in HCC827 NSCLC cells due to induction of cell death and active caspase-3/8 activities by AZD5582 and IFNγ co-treatment
- Causes degradation of cIAP1 and caspase 3 cleavage in tumor cells in MDA-MB-231 xenograft-bearing mice
Medchemexpress LLC AZD5582 dihydrochloride | 1883545-51-4 | 99.8% | 1088.21 | 1 ML
AZD5582 dihydrochloride is an antagonist of the inhibitor of apoptosis proteins (IAPs). It binds to the BIR3 domains of cIAP1, cIAP2, and XIAP with IC50s of 15 nM, 21 nM, and 15 nM, respectively, and induces apoptosis. It inhibits cell viability in cooperation with IFNγ or viral double-stranded RNA (dsRNA) in H1975 NSCLC cells. It also downregulates cIAP-1, activates RIPK1 (upstream regulator of caspase-8), and triggers the activation of extrinsic (caspase-8) and intrinsic (caspase-9) apoptosis pathways, leading to the cleavage of caspase-3 and caspase-7.
- Antagonist of inhibitor of apoptosis proteins (IAPs).
- Binds to BIR3 domains of cIAP1, cIAP2, and XIAP.
- Induces apoptosis.
- Inhibits cell viability in NSCLC cells.
- Downregulates cIAP-1 and activates RIPK1.
- Triggers extrinsic and intrinsic apoptosis pathways.