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AD-2646 has antidepressant activity and inhibits 2-deoxy-D-glucose (2-DG)-induced gastric acid secretion.

AD-2646 FA has antidepressant activity and inhibits 2-deoxy-D-glucose (2-DG)-induced gastric acid secretion.

CRANAD-28 is a blood-brain barrier (BBB) penetrating two-photon imaging probe capable of visualizing amyloid plaques and labeling plaques and cerebral amyloid angiopathy.

USP7-IN-4(USP7 inhibitor ALM4) is a non-competitive, potent and selective inhibitor of USP7 (ubiquitin-specific protease 7) with an IC50 = 6 nM, up-regulates p53 and p21, down-regulates MDM2, increases the level of ubiquitination of MDM2, and exhibits anti-proliferative activity in a variety of cancer cell lines, with an EC50 = 2.0 nM in RS4;11 (acute lymphoblastic leukemia cell line) .

Alisertib (MLN 8237) is a specific Aurora A inhibitor (IC50: 1.2 nM). The selectivity of Alisertib(MLN 8237) is >200-fold higher for Aurora A than Aurora B.

1. Orientin (Luteolin-8-glucoside) may be regarded as a candidate therapeutic agent for treatment of vascular inflammatory diseases via inhibition of the HMGB1 signaling pathway. 2. Orientin protects vascular barrier integrity by inhibiting hyperpermeability, expression of CAMs, and adhesion and migration of leukocytes, thereby endorsing its usefulness as a therapy for vascular inflammatory diseases. 3. Orientin has neuroprotection effect by the intracellular mediation of caspase activity; may alleviate cognitive deficits and oxidative stress in AD mice; can exert antidepressant-like effects on CUMS mice, specifically by improving central oxidative stress, neurotransmission, and neuroplasticity.

(1S,2R)-Alicapistat ((1S,2R)-ABT-957) is a highly efficient, orally active compound that selectively inhibits human calpains 1 and 2, showing promise for Alzheimer's disease (AD) therapy [1]. It effectively addresses the metabolic liability associated with carbonyl reduction and demonstrates potent inhibition of calpain 1 with an IC50 value of 395 nM [2].

Alicapistat (ABT-957) is a human calpains 1 and 2 inhibitor. It can potentially be used to treat Alzheimer's disease (AD).

GSK-3β inhibitor24 (Compound 41) is a potent GSK-3β inhibitor with an IC50 of 0.22 nM. It increases GSK-3β phosphorylation at the Ser9 site in a dose-dependent manner and inhibits tau protein hyperphosphorylation by reducing the abundance of p-tau-Ser396. The compound upregulates β-catenin and neurogenesis-related markers (GAP43 and MAP-2), demonstrating significant anti-Alzheimer's disease (AD) activity.

BF-170 is a selective tau fiber-binding agent with an EC50 of 221 nM. It demonstrates excellent blood-brain barrier penetration, reaching a concentration of 9.1% ID g in brain tissue 2 minutes after intravenous injection in mice (with a clearance rate of 0.25% ID g at 30 minutes). BF-170 can serve as a probe for imaging tau protein pathology in Alzheimer's disease (AD). It plays a significant role in early-stage Alzheimer's disease studies and holds promise for imaging research in tau-related neurodegenerative diseases.

Ensaculin is a NMDA antagonist and a 5HT1A agonist potentially for the treatment of Alzheimer's disease (AD). Ensaculin showed memory-enhancing effects in paradigms of passive and conditioned avoidance in both normal and artificially amnesic rodents. It e

SAR502250 is a potent, selective, ATP-competitive, orally active, and brain-penetrant GSK3 inhibitor with a human GSK-3β IC50 value of 12 nM, exhibiting antidepressant-like activity and being researched for potential application in Alzheimer's disease (AD) treatment.

Zonisamide-13C2,15N is intended for use as an internal standard for the quantification of zonisamide by GC- or LC-MS. Zonisamide is an antiepileptic agent.1 It selectively inhibits the repeated firing of sodium channels (IC50 = 2 μg/ml) in mouse embryo spinal cord neurons and inhibits spontaneous channel firing when used at concentrations greater than 10 μg/ml.2 In rat cerebral cortex neurons, zonisamide (1-1,000 μM) inhibits T-type calcium channels with a maximum reduction of 60% of the calcium current.3 Zonisamide inhibits H. pylori recombinant carbonic anhydrase (CA) and the human CA isoforms I, II, and V with Ki values of 218, 56, 35, and 21 nM, respectively.4,5 In mice, it has anticonvulsant activity against maximal electroshock seizure (MES) and pentylenetetrazole-induced maximal, but not minimal, seizures (ED50s = 19.6, 9.3, and >500 mg/kg, respectively). Zonisamide (40 mg/kg, p.o.) prevents MPTP-induced decreases in the levels of dopamine , but not homovanillic acid or dihydroxyphenyl acetic acid , and increases MPTP-induced decreases in the dopamine turnover rate in mouse striatum in a model of Parkinson's disease.6 Formulations containing zonisamide have been used in the treatment of partial seizures in adults with epilepsy. |1. Masuda, Y., Ishizaki, M., and Shimizu, M. Zonisamide: Pharmacology and clinical efficacy in epilepsy. CNS Drug Rev. 4(4), 341-360 (1998).|2. Rock, D.M., Macdonald, R.L., and Taylor, C.P. Blockade of sustained repetitive action potentials in cultured spinal cord neurons by zonisamide (AD 810, CI 912), a novel anticonvulsant. Epilepsy Res. 3(2), 138-143 (1989).|3. Suzuki, S., Kawakami, K., Nishimura, S., et al. Zonisamide blocks T-type calcium channel in cultured neurons of rat cerebral cortex. Epilepsy Res. 12(1), 21-27 (1992).|4. Nishimori, I., Vullo, D., Minakuchi, T., et al. Carbonic anhydrase inhibitors: Cloning and sulfonamide inhibition studies of a carboxyterminal truncated α-carbonic anhydrase from Helicobacter pylori. Bioorg. Med. Chem. Lett. 16(8), 2182-2188 (2006).|5. De Simone, G., Di Fiore, A., Menchise, V., et al. Carbonic anhydrase inhibitors. Zonisamide is an effective inhibitor of the cytosolic isozyme II and mitochondrial isozyme V: Solution and X-ray crystallographic studies. Bioorg. Med. Chem. Lett. 15(9), 2315-2320 (2005).|6. Yabe, H., Choudhury, M.E., Kubo, M., et al. Zonisamide increases dopamine turnover in the striatum of mice and common marmosets treated with MPTP. J. Pharmacol. Sci. 110(1), 64-68 (2009).

LEO 39652, a dual-soft PDE4 inhibitor, demonstrates potent inhibition of PDE4 subtypes A, B, C, and D with respective IC50 values of 1.2 nM, 1.2 nM, 3.0 nM, and 3.8 nM. Additionally, it inhibits TNF-α with an IC50 of 6.0 nM, indicating its potential for topical Atopic dermatitis (AD) research [1].

BChE-IN-2 (compound 22) is a highly effective inhibitor of BChE, with a Ki value of 0.099 μM, and represents a promising pyrimidine and pyridine derivative for investigating Alzheimer's disease (AD). [1]

BChE-IN-6 (compound 12) is a highly effective inhibitor of BChE with a Ki value of 0.182 μM, and it exhibits significant chelating abilities towards Zn 2+. These characteristics make BChE-IN-6 a valuable tool for researchers in the field of Alzheimer's disease (AD) [1].

AChE BChE-IN-2 (Compound 13b) is a potent inhibitor of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), exhibiting IC50 values of 0.96 ± 0.14 μM for AChE and 1.23 ± 0.23 μM for BChE.

5-{8-[(3,4'-Difluoro[1,1'-biphenyl]-4-yl)methoxy]-2-methylimidazo[1,2-a]pyridin-3-yl}-N-methylpyridine-2-carboxamide (1o) exhibited high in vitro potency and brain exposure, significantly reduced brain Aβ42 levels, showed no inhibitory effect on cytochrome p450 enzymes, and demonstrated excellent anti-cognitive deficits in AD model mice.

WF-47-JS03 is a selective and potent inhibitor of RET kinase that crosses the blood-brain barrier and is more than 500-fold more selective for the kinase insertion domain receptor (KDR).WF-47-JS03 acts on Ba F3 cells transfected with KIF5B-RET (IC50: 1.7 nM) and LC-2 ad lung cancer cells transfected with CCDC6-RET (IC50: 5.3 nM). cells (IC50: 5.3 nM).

RET-IN-11 is a potent and selective RET inhibitor that acts on RET (IC50: 6.20 nM) and RETV804M (IC50: 18.68 nM). RET-IN-11 induces apoptosis and exhibits anti-proliferative and migratory effects in LC-2 ad cells.

NXPZ-2 is an orally active Keap1-Nrf2 protein-protein interaction (PPI) inhibitor (Ki: 95 nM, EC50: 120 and 170 nM). NXPZ-2 dose-dependently attenuates Aβ[1-42]-induced cognitive disturbances, enhances neuronal number and function, and improves pathological alterations in the brain of Alzheimer's disease (AD) mice. NXPZ-2 has potential for studies of Keap1-Nrf2 PPI inhibitors and AD-related disorders.

AChE BuChE-IN-1, a selective butyrylcholinesterase (BuChE) inhibitor derived from chrysin, exhibits a potent efficacy with an IC50 of 0.48 μM against BuChE and a lesser inhibitory effect on acetylcholinesterase (AChE) with an IC50 of 7.16 μM. It demonstrates significant hydroxyl radical (·OH) scavenging activity, achieving an IC50 of 0.1674 μM, and effectively inhibits reactive oxygen species (ROS) and Aβ 1-42 aggregation, including self-aggregation, copper (Cu 2+)-induced, and AChE-induced aggregation. Characterized by high blood-brain barrier (BBB) permeability, bioavailability, and low cellular toxicity, AChE BuChE-IN-1 holds promising potential for Alzheimer's disease (AD) research.

sEH AChE-IN-2 and acetylcholinesterase ( AChE ). sEH AChE-IN-2 provides cumulative effects against neuroinflammation and memory impairment. sEH AChE-IN-2 has the potential for the research of Alzheimer's disease (AD) .

Prostaglandin J2 (PGJ2), a derivative of Prostaglandin D2 (PGD2), serves as a potent agonist for PGD2 receptors (DP), exhibiting affinity constants (K i) of 0.9 nM and 6.6 nM for hDP and hCRTH2 receptors, respectively. It activates cyclic AMP production with an EC50 of 1.2 nM, induces oxidative stress, neuronal apoptosis, and promotes the accumulation of ubiquitinated (Ub) proteins. Notably, PGJ2's neurotoxic properties are implicated in the progression of neurodegenerative diseases such as Alzheimer's (AD) and Parkinson's (PD) [1] [2] [3] [4].