peak

NS5806 是钾电流的激活剂，可增加 KV4.3/KChIP2峰值电流幅度，EC50值为 5.3 μM。它会在包含 KChIP2 的通道复合体中降低 KV4.2 和 KV4.3 电流衰减。

22393-62-0_peak 2 exhibits some aspects of the antiestrogenic activity and other actions that may be connected to the estrogenic properties. A mixture of the (Z)- and (E)-isomers (Broparestrol, INN) is used in dermatology.

1,1'-Ethylidene-bis-(L-tryptophan) is a potential impurity in L-tryptophan commercial products, promoting EoL-3 eosinophilic leukemia cell proliferation, enhancing eosinophil cationic protein release from human peripheral blood eosinophils, and boosting IL-5 production in human T cells. At 40 µg kg, it triggers fascia thickening, mast cell infiltration, inflammation, and fibrosis in mouse superficial adipose and panniculus carnosus tissues, serving as an eosinophilia-myalgia syndrome research model.

AZD-1305是一种新型抗心律失常化合物，主要阻断哺乳动物细胞和心室心肌细胞中 IKr 的快速组分、l 型钙电流和病房内钠电流，可用于研究逆转心律失常。

TPO-L是一种用于紫外光(UV)固化和3D打印的自由基光引发剂，对长波紫外光具有优异的吸收性能，能快速引发单体和齐聚物的聚合反应。

U93631 是一种具有新型化学结构的 GABAA 受体配体，IC50 为 100 nM，它在重组 GABAA 受体中诱导 GABA 诱导的全细胞 Cl 电流快速，这种效果随时间依赖性衰减。

(-)-Cevimeline hydrochloride hemihydrate ((-)-SNI-2011) 是一种新型mAChR 激动剂，是一种治疗干燥综合征口干症的候选治疗药物。

(+)-Cevimeline hydrochloride hemihydrate ((+)-SNI-2011) 是一种有效的 mAChR 激动剂。

The peak excitation and emission wavelengths of EC-17 are 470 520 nm.EC-17 (disodium salt) is a folate receptor alpha (FRα) targeting contrast agent with fluorescent properties in the visible light spectrum.

Antitumor agent-187（compound I3），是一种基于5,15-二芳基四苯并卟啉的光敏剂，具抗癌特性且其最大吸收波长约为668 nm。该化合物在光动力疗法（PDP）中发挥作用，能诱导癌细胞凋亡，并优先在肿瘤位置累积，同时具备实时荧光成像的功能。

Protoporphyrin IX disodium 作为辐射敏化剂，在缺氧环境下能有效增强 ROS 的生成并诱导 DNA 损伤。作为光敏剂，该化合物在光照射下可经历光漂白反应直接降解。此外，Protoporphyrin IX disodium 能在大鼠肿瘤细胞中通过给药 5-aminolevulinic acid (5-ALA) 形成并积累。在 405 nm 波长的红色荧光激活下，它可有效改善基底细胞癌的病情。Protoporphyrin IX disodium 在声动力和光动力疗法中对治疗膀胱癌和结节性基底细胞癌具有研究潜力。

(±)-Penbutolol ((Rac)-Penbutolol) 属于Penbutolol的外消旋体。作为一种β-肾上腺素受体拮抗剂，其具备口服活性。该化合物能有效抑制运动引起的心动过速，降低运动时的峰值呼气流量（PEFR）并在静息状态下减少肾素活性（PRA）。服用后1小时内，(±)-Penbutolol在血液中达到峰值浓度，半衰期为4.5小时，并转化为活性代谢物。该化合物常用于心血管病的相关研究。

Pirquinozol (SQ 13,847) 是一种口服有效的抗过敏剂，其通过转化为氧化代谢物 SQ 12,903 发挥最大活性。Pirquinozol 能够抑制大鼠的支气管痉挛。

GABAA receptor modulator-3 (compound 3b) 是一种正向变构调节剂 (PAM)。该化合物抑制α1β3γ2 GABAAR的峰值电流和稳态电流，IC50值分别为671 μM和64 μM。

GABAA receptor modulator-4 (Compound 4) 为 GABAA 受体 (GABAA receptor) 的负向变构调节剂，它抑制 α1β3γ2 GABAA 受体介导的峰值和稳态电流，IC50均为 10 μM。

Nav1.2-IN-1 (compound 5i) 是一种 3-(1,2,3,6-tetrahydropyridine)-4-azaindole 衍生物，具高效性和选择性，可作为 Nav1.2 的抑制剂。该化合物能降低 Nav1.2 电流峰值，IC50 值为 7.79 μM，并展现抗癫痫活性。在皮下注射戊四氮 (sc-PTZ) 诱发的癫痫模型中，它展现出优异的抗惊厥效果且神经毒性低。

JNJ-55511118 是一种具有高效性和选择性的 TARP γ8 负变构调节剂，具有抗惊厥和神经保护活性，通过降低其单通道电导来抑制含有 γ8 的 AMPAR 的峰值电流，可用于研究慢性操作性酒精自我给药。

BMS-902483 is a potent α7 partial agonist. BMS-902483 improved cognition in preclinical rodent models. BMS-902483 showed FLIR α7 EC50=9.3nM; α7 Electrophysiology, rat; Area EC50 = 140 nM; Peak, Area (Ymax %) = 40, 54. 5-HT3A IC50 = 480 nm.

R-1663 is a factor Xa inhibitor. R-1663 prolonged clotting times, inhibited thrombin generation (peak height and endogenous thrombin potential [ETP]) and anti-factor Xa activity in a concentration-dependent manner without increasing bleeding time. Pharmac

KT 1 decreased aortic pressure, renal blood flow, left ventricular enddiastolic pressure and resistances of total peripheral, vertebral, coronary and renal vasculatures and increased aortic blood flow, vertebral blood flow, coronary blood flow, peak posit

Massarigenin C is a fungal metabolite that has been found inM. flavoroseaand has enzyme inhibitory activities.1,2Massarigenin C inhibits neuraminidasein vitro(IC50= 4.15 μM).2It is also an inhibitor of yeast α-glucosidase (IC50= 1.25 mM).1It reduces the postprandial peak in blood glucose levels in an oral sucrose tolerance test in normo- and hyperglycemic mice when administered at doses of 3.2, 10, and 31.6 mg kg.

ARN-21934 是高选择性的人拓扑异构酶 II α 抑制剂，具有血脑屏障通透性。依托泊苷抑制 DNA 松弛的IC50为120 μM，ARN-21934 抑制 DNA 松弛的IC50为 2 μM。ARN-21934具有良好的体内药代动力学特性。

Aspergillimide is a fungal metabolite originally isolated from A. japonicus.1 It reduces nicotinic acetylcholine receptor (nAChR) peak and slowly-desensitizing amplitudes induced by acetylcholine in silkworm (B. mori) larval neurons (IC50s = 20.2 and 39.6 nM, respectively) but has no effect on chicken α3β4-, α4β2-, and α7-containing nAChRs.2 Dietary administration of aspergillimide A (10 μg/g of diet) induces paralysis in silkworm fourth instar larvae.1 Aspergillimide A (10 and 20 mg/kg) reduces T. colubriformis fecal egg count in gerbils.3References1. Hayashi, H., Nishimoto, Y., Akiyama, K., et al. New paralytic alkaloids, asperparalines A, B and C, from Aspergillus japonicus JV-23. Biosci. Biotechnol. Biochem. 64(1), 111-115 (2000).2. Hirata, K., Kataoka, S., Furutani, S., et al. A fungal metabolite asperparaline a strongly and selectively blocks insect nicotinic acetylcholine receptors: The first report on the mode of action. PLoS One 6(4), e18354 (2011).3. Banks, R.M., Blanchflower, S.E., Everett, J.R., et al. Novel anthelmintic metabolites from an Aspergillus species; the aspergillimides. J. Antibiot. (Tokyo) 50(10), 840-846 (1997). Aspergillimide is a fungal metabolite originally isolated from A. japonicus.1 It reduces nicotinic acetylcholine receptor (nAChR) peak and slowly-desensitizing amplitudes induced by acetylcholine in silkworm (B. mori) larval neurons (IC50s = 20.2 and 39.6 nM, respectively) but has no effect on chicken α3β4-, α4β2-, and α7-containing nAChRs.2 Dietary administration of aspergillimide A (10 μg/g of diet) induces paralysis in silkworm fourth instar larvae.1 Aspergillimide A (10 and 20 mg/kg) reduces T. colubriformis fecal egg count in gerbils.3 References1. Hayashi, H., Nishimoto, Y., Akiyama, K., et al. New paralytic alkaloids, asperparalines A, B and C, from Aspergillus japonicus JV-23. Biosci. Biotechnol. Biochem. 64(1), 111-115 (2000).2. Hirata, K., Kataoka, S., Furutani, S., et al. A fungal metabolite asperparaline a strongly and selectively blocks insect nicotinic acetylcholine receptors: The first report on the mode of action. PLoS One 6(4), e18354 (2011).3. Banks, R.M., Blanchflower, S.E., Everett, J.R., et al. Novel anthelmintic metabolites from an Aspergillus species; the aspergillimides. J. Antibiot. (Tokyo) 50(10), 840-846 (1997).

OPC-167832 is a potent and orally active dprE1 Inhibitor with an IC50 of 0.258 μM. OPC-167832 has antituberculosis activity and can be used for the research of tuberculosis caused by Mycobacterium tuberculosis[1]. OPC-167832 exhibits very low MICs against laboratory strains of M. tuberculosis H37Rv (MIC: 0.0005 μg ml) and Kurono (MIC: 0.0005 μg ml) and strains with monoresistance to rifampin (RIF), isoniazid (INH), ethambutol (EMB), streptomycin (STR), and pyrazinamide (PZA) (MIC: 0.00024-0.001 μg ml). However, OPC-167832 has minimal or no activity against standard strains of nonmycobacterial aerobic and anaerobic bacteria[1].The IC90 values of OPC-167832 against intracellular M. tuberculosis strains H37Rv and Kurono are 0.0048 and 0.0027 μg ml, respectively. OPC-167832 shows bactericidal activity against intracellular M. tuberculosis at a low concentration, and the bactericidal activity is saturated at concentrations of 0.004 μg ml or higher[1]. OPC-167832 (oral administration; 0.625-10 mg kg) exhibits a good pharmacokinetic characteristic. The plasma reaches peak at 0.5 h to 1.0 h (tmax) and is eliminated with a half-life (t1 2) of 1.3 h to 2.1 h OPC-167832 distribution in the lungs is approximately 2 times higher than that in plasma, and the Cmax and AUCt of OPC-167832 in plasma and the lungs shows dose dependency[1].OPC-167832 (oral administration; 0.625-10 mg kg; 4 weeks) significantly reduces lung CFU compared to the vehicle group. The dose-dependent decrease of lung CFU is observed from 0.625 mg kg to 2.5 mg kg. In a M. tuberculosis Kurono-infected ICR female mice model. OPC-167832 combines with DMD, BDQ, or LVX via oral gavage exhibits significantly higher efficacies than each single agent alone[1].[1].OPC-167832 (oral gavage; 2.5 mg kg; combination with DCMB; 12 weeks) demonstrates the most potent efficacy when compares with DC, DCB. The lung CFU count after 6 weeks of treatment is below the detection limit, and at the end of just 8 weeks of treatment, the bacteria in the lungs of all the evaluated mice had already been eradicate[1]. [1]. Norimitsu Hariguchi, et al. OPC-167832, a Novel Carbostyril Derivative with Potent Antituberculosis Activity as a DprE1 Inhibitor.Antimicrob Agents Chemother. 2020 May 21;64(6):e02020-19.