Heart Failure Research
Heart failure, also known as congestive heart failure or CHF, is an inability of the heart to pump sufficient blood around the body.Heart failure typically occurs secondary to an existing pathology that alters cardiac function. Examples of syndromes that can precede heart failure include myocardial infarction, arrhythmia or infection. These can also cause dilated cardiomyopathy, a condition which accounts for approximately one third of all cases of heart failure. The pathogenesis of heart failure is cyclical and progressive; endogenous mechanisms, which are activated during heart failure in an attempt to counteract the symptoms, actually worsen cardiac function. Cardiac dysfunction, either systolic or diastolic, triggers a decrease in stroke volume and a resultant increase in cardiac output. In healthy individuals the body responds to decreases in cardiac output by initiating the renin-angiotensin-aldosterone system (RAAS) to promote fluid retention, and also by activating the sympathetic nervous system to cause peripheral vasoconstriction. Under normal circumstances this counteracts the imbalance in stroke volume, restoring cardiac output to normal levels. In patients with heart failure the increase in blood volume, together with the heightened peripheral resistance and elevated levels of circulating catecholamines, causes an increased load on the already weakened ventricles with each contraction, and the stroke volume does not return to normal levels. Repeated cycles of this process further weaken the ventricle walls, prompting ventricular hypertrophy and a decreased force of contraction.
Heart Failure Research Products Targets
- PI 3-kinase (22)
- Others (7)
- Mineralocorticoid Receptor (7)
- Angiotensin-Converting Enzyme (8)
- NO donors and precursors (9)
- nNOS (5)
- iNOS (11)
- eNOS (1)
- Angiotensin AT2 Receptor (3)
- Angiotensin AT1 Receptor (9)
- NKCC (2)
- Adrenergic α2 Receptor (33)
- Adrenergic α1 Receptor (22)
- Adrenergic β2 Receptor (6)
- Adrenergic β1 Receptor (7)
Products for Heart Failure Research - Page 10
- Cat.No. Product Name Information/Activity
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BCC1110
KU-0060648
KU-0060648 is a dual inhibitor of PI3K and DNA-PK with IC50s of 4 nM, 0.5 nM, 0.1 nM, 0.594 nM and 8.6 nM for PI3Kα, PI3Kβ, PI3Kγ, PI3Kδ and DNA-PK, respectively.
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BCC1715
LY 303511
LY303511 is a structural analogue of LY294002. LY303511 does not inhibit PI3K. LY303511 enhances TRAIL sensitivity of SHEP-1 neuroblastoma cells. LY303511 reversibly blocks K+ currents (IC50=64.6±9.1 μM) in MIN6 insulinoma cells.
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BCC3714
3-Methyladenine
3-Methyladenine is a PI3K inhibitor. 3-Methyladenine is a widely used inhibitor of autophagy via its inhibitory effect on class III PI3K.
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BCC3837
PF-04691502
PF-04691502 is a potent and selective inhibitor of PI3K and mTOR. PF-04691502 binds to human PI3Kα, β, δ, γ and mTOR with Kis of 1.8, 2.1, 1.6, 1.9 and 16 nM, respectively.
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BCC4987
PF-05212384 (PKI-587)
Gedatolisib (PKI-587) is a highly potent dual inhibitor of PI3Kα, PI3Kγ, and mTOR with IC50s of 0.4 nM, 5.4 nM and 1.6 nM, respectively. PKI-587 is equally effective in both complexes of mTOR, mTORC1 and mTORC2.
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BCC1860
PI-103 Hydrochloride
PI-103 Hydrochloride is a dual PI3K and mTOR inhibitor with IC50s of 8 nM, 88 nM, 48 nM, 150 nM, 20 nM, and 83 nM for p110α, p110β, p110δ, p110γ, mTORC1, and mTORC2. PI-103 Hydrochloride also inhibits DNA-PK with an IC50 of 2 nM. PI-103 Hydrochloride induces autophagy.
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BCC5379
PI-3065
PI-3065 is a potent inhibitor of PI3K p110δ, with IC50 and Ki values of 5 nM and 1.5 nM, and exhibits less potent activity against p110α, p110β, p110γ with IC50s of 910, 600, >10000 nM.
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BCC7494
PI 828
PI-828 is a dual PI3K and casein kinase 2 (CK2) inhibitor with IC50s of 173 nM, 149 nM, and 1127 nM for p110α, CK2, and CK2α2 in lipid kinase assay, respectively.
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BCC4980
PP121
PP121 is a multi-targeted kinase inhibitor with IC50s of 10, 60, 12, 14, 2 nM for mTOR, DNK-PK, VEGFR2, Src, PDGFR, respectively.
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BCN6049
Quercetin
Quercetin, a natural flavonoid, is a stimulator of recombinant SIRT1 and also a PI3K inhibitor with IC50 of 2.4±0.6 μM, 3.0±0.0 μM and 5.4±0.3 μM for PI3K γ, PI3K δ and PI3K β, respectively.


