is-145

IS-145 is a thromboxane A2 receptor antagonist.

QQN-00358 is a novel potent and selective tankyrase (TNKS) inhibitor.

CDK9-IN-7 (compound 21e) 是一种高效选择性的，具有口服活性的 CDK9 cyclin T 抑制剂 (IC50=11 nM)，与抑制其他 CDK 相比更有效 (CDK4 cyclinD=148 nM; CDK6 cyclinD=145 nM)。CDK9-IN-7 具有抗癌活性并没有明显的毒性。CDK9-IN-7 诱导非小细胞肺癌 (NSCLC) 细胞凋亡，在 G2 期阻滞细胞周期，并具有抑制非小细胞肺癌干细胞特性。

MSC2360844 是一种选择性的、具有口服活性的PI3Kδ抑制剂，其 IC50=145 nM。它对一组 278 种其他激酶显示出高度选择性。

Duvelisib (INK1197， IPI-145）是磷脂酰肌醇-3激酶（PI3K）和 p100δ的选择性抑制剂，能够作用于 p110δ (IC50值为0.0025 μM)、p110γ (IC50值为0.274 μM)、p110β (IC50值为0.85 μM) 和 p110α (IC50值为1.602 μM)。

Lidocaine (Alphacaine) 是一种酰胺衍生物，抑制涉及复杂电压和依赖性的钠通道，可用于研究室性心律失常。它通过调节 miR-145 表达和进一步抑制 MEK ERK 和 NF-κB 信号通路来减少胃癌细胞的生长，迁移和侵袭。

Lidocaine hydrochloride (Lignocaine hydrochloride) 抑制涉及复杂电压和依赖性的钠通道。它通过调节 miR-145 表达和进一步抑制 MEK ERK 和 NF-κB 信号通路来减少胃癌细胞的生长，迁移和侵袭。Lidocaine 是一种酰胺衍生物，是一种研究室性心律失常的药物和有效的肿瘤抑制剂。

Duvelisib R enantiomer (IPI-145 R enantiomer) 是一种 Duvelisib 的对映异构体，活性较低。 它是一种 PI3K 抑制剂。

FAAH-IN-1 is a fatty acid amide hydrolase (FAAH) inhibitor, with IC50s of 145 nM and 650 nM for rat and human FAAH, respectively.

ML 145 是一种具有选择性和高效性的人 GPR35 拮抗剂，对啮齿动物直系同源物的 GPR35 均无明显活性。ML 145 具有潜在的抗炎活性，可用于研究免疫炎症。

Mps1-IN-2 是一种 ATP 竞争性Mps1 Plk1选择性双重抑制剂，对 Mps1 的IC50和Kd 值分别为 145 和 12 nM，对 Plk1 的Kd 值为 61 nM。

GSTP1-1 inhibitor 2 (Compound 5g) 作为hGSTP1-1(谷胱甘肽转移酶 P1-1)的有效抑制剂，其IC50为12.2 μM。此化合物对 DU-145、PC3 和 MCF-7 细胞系显示出较强的细胞毒性，其CC50值分别为36.6、11.9 和 17.4 μM，显示其在抗癌研究领域的潜在应用价值。

E3 Ligase Ligand-linker Conjugate 145 是一种E3泛素连接酶配体和接头的结合物，用于合成PROTACAR Degrader-7。

Aurora A inhibitor4 (compound C9) 是一种Aurora A的高效抑制剂，在DU 145细胞和HT-29细胞中的GI50值分别为4.26 μM和7.08 μM。

EGFR-IN-145 (compound 7c) 是一款EGFR激酶抑制剂。在20 μM浓度下，其对EGFR野生型激酶的抑制率达到52.7%。

Anticanceragent 264 (Compound 5w) 是一种抗癌剂，在多种肿瘤细胞系中展现出明显的抗增殖活性，IC50范围为7.5-33.67 μM。它能显著诱导MDA-MB-231、MIA PaCa-2和DU-145细胞系在G2 M期的细胞周期停滞，并以剂量依赖性方式降低关键细胞周期蛋白CDK1、CDK2和Cyclin B1。该化合物与分化抑制剂和DNA结合蛋白表现出良好的结合活性，适用于癌症相关领域的研究。

CYP17A1-IN-1 (Compound 14) 为CYP17A1的抑制剂，其IC50为26 nM。在雄激素敏感的前列腺癌细胞LNCaP中表现出细胞毒性，并抑制细胞DU-145的迁移。

MMP-145 is used as a protease inhibitor.

Ioforminol, also known as GE-145 and AN-113111, is a new low-osmolar dimeric radiographic contrast agent. GE-145 exhibits similar preclinical properties to other dimeric radiographic contrast media. In addition, the low osmolality enables an iso-osmolar f

Panduratin A(泛影素 A)是一种天然的查尔酮衍生物，在人口腔表皮样癌KB细胞中对MMP-9具有抑制活性；对DENV-2的NS3蛋白酶具有抑制活性（Ki=25 μM）；对人雄激素非依赖性前列腺癌细胞PC-3和DU-145有明显的细胞毒性；还能够激活LKB1-AMPK-PPARα δ信号通路，增强肌细胞线粒体的氧化能力。

Kisspeptin-54 is a peptide ligand of the orphan G protein-coupled receptor GPR54 (Kis = 1.81 and 1.45 nM for rat and human receptors, respectively).1 It is a 54 amino acid peptide encoded by the metastasis suppressor gene KISS-1. Kisspeptin-54 induces calcium mobilization in CHO-K1 cells expressing rat and human receptors (EC50s = 1.39 and 5.47 nM, respectively). It also induces arachidonic acid release in CHO cells expressing rat and human GPR54 in a concentration-dependent manner. Kisspeptin-54 (10-1,000 nM) inhibits insulin secretion from isolated mouse pancreatic β-cells in the presence of 2.8 mM, but not 11.1 mM, glucose.2 Kisspeptin-54 (1-5 nmol, i.c.v.) increases serum levels of luteinizing hormone (LH) and follicular stimulating hormone (FSH) in mice, an effect which is reversed by the gonadotropin releasing hormone (GNRH) antagonist acycline.3References1. Kotani, M., Detheux, M., Vandenbogaerde, A.L., et al. The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54. J. Biol. Chem. 276(37), 34631-34636 (2001).2. Vikman, J., and Ahrén, B. Inhibitory effect of kisspeptins on insulin secretion from isolated mouse islets. Diabetes Obes. Metab. 11(Suppl 4), 197-201 (2009).3. Gottsch, M.L., Cunningham, M.J., Smith, J.T., et al. A role for kisspeptins in the regulation of gonadotropin secretion in the mouse. Endocrinology 145(9), 4073-4077 (2004). Kisspeptin-54 is a peptide ligand of the orphan G protein-coupled receptor GPR54 (Kis = 1.81 and 1.45 nM for rat and human receptors, respectively).1 It is a 54 amino acid peptide encoded by the metastasis suppressor gene KISS-1. Kisspeptin-54 induces calcium mobilization in CHO-K1 cells expressing rat and human receptors (EC50s = 1.39 and 5.47 nM, respectively). It also induces arachidonic acid release in CHO cells expressing rat and human GPR54 in a concentration-dependent manner. Kisspeptin-54 (10-1,000 nM) inhibits insulin secretion from isolated mouse pancreatic β-cells in the presence of 2.8 mM, but not 11.1 mM, glucose.2 Kisspeptin-54 (1-5 nmol, i.c.v.) increases serum levels of luteinizing hormone (LH) and follicular stimulating hormone (FSH) in mice, an effect which is reversed by the gonadotropin releasing hormone (GNRH) antagonist acycline.3 References1. Kotani, M., Detheux, M., Vandenbogaerde, A.L., et al. The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54. J. Biol. Chem. 276(37), 34631-34636 (2001).2. Vikman, J., and Ahrén, B. Inhibitory effect of kisspeptins on insulin secretion from isolated mouse islets. Diabetes Obes. Metab. 11(Suppl 4), 197-201 (2009).3. Gottsch, M.L., Cunningham, M.J., Smith, J.T., et al. A role for kisspeptins in the regulation of gonadotropin secretion in the mouse. Endocrinology 145(9), 4073-4077 (2004).

PAR2 (1-6) amide is a synthetic peptide agonist of proteinase-activated receptor 2 (PAR2) that corresponds to residues 1-6 of the amino terminal tethered ligand sequence of human PAR2 and residues 37-42 of the full-length sequence.1It binds to NCTC 2544 cells expressing human PAR2 (Ki= 9.64 μM in a radioligand binding assay) and induces calcium mobilization in the same cells (EC50= 0.075 μM).2PAR2 (1-6) amide (100 μM) reduces colony formation of A549 lung cancer cells.1It induces superoxide production and degranulation in isolated human eosinophils when used at a concentration of 500 μM.3PAR2 (1-6) amide (5 μmol kg) induces tear secretion in rats when used in combination with amastatin .4 1.Bohm, S.K., Kong, W., Bromme, D., et al.Molecular cloning, expression and potential functions of the human proteinase-activated receptor-2Biochem. J.314(Pt 3)1009-1016(1996) 2.Kanke, T., Ishiwata, H., Kabeya, M., et al.Binding of a highly potent protease-activated receptor-2 (PAR2) activating peptide, [3H]2-furoyl-LIGRL-NH2, to human PAR2Br. J. Pharmacol.145(2)255-263(2005) 3.Miike, S., McWilliam, A.S., and Kita, H.Trypsin induces activation and inflammatory mediator release from human eosinophils through protease-activated receptor-2J. Immunol.167(11)6615-6622(2001) 4.Nishikawa, H., Kawai, K., Tanaka, M., et al.Protease-activated receptor-2 (PAR-2)-related peptides induce tear secretion in rats: Involvement of PAR-2 and non-PAR-2 mechanismsJ. Pharmacol. Exp. Ther.312(2)324-331(2005)

Terpendole I is a fungal metabolite that has been found in A. yamanashiensis.1 It is a weak inhibitor of acyl-coenzyme A:cholesterol acyltransferase (ACAT; IC50 = 145 μM) and is active against the bacteria B. cereus and B. subtilis (MICs = 100 μg/ml for both) but not S. aureus, P. aeruginosa, or K. pneumoniae (MICs = >200 μg/ml for all) or the fungus C. albicans (MIC = 200 μg/ml).1,2 It is cytotoxic to HeLa cells with an IC50 value of 52.6 μM.3 |1. Tomoda, H., Tabata, N., Yang, D.-J., et al. Terpendoles, novel ACAT inhibitors produced by Albophoma yamanashiensis. III. Production, isolation and structure elucidation of new components. J. Antibiot. (Tokyo) 48(8), 793-804 (1995).|2. Zhao, J.-C., Wang, Y.-L., Zhang, T.-Y., et al. Indole diterpenoids from the endophytic fungus Drechmeria sp. as natural antimicrobial agents. Phytochemistry 148, 21-28 (2018).|3. Nagumo, Y., Motoyama, T., Hayashi, T., et al. Structure-activity relationships of terpendole E and its natural derivatives. ChemistrySelect 2(4), 1533-1536 (2017).

MSA-2 dimer is a selective, orally active non-nucleotide STING agonist (Kd=145 μM) with long-term antitumor and immunogenic activity. MSA-2 dimer is bound to STING as a non-covalent dimer exhibiting higher permeability than cyclic dinucleotide[1]. MSA-2 dimer (60 mg kg; p.o.; 50 days) inhibits tumor growth and prolongs overall survival[1]. MSA-2 dimer (40 mg kg; s.c.; 25 days) induces complete tumor regression[1].MSA-2 dimer (60 mg kg; p.o.; 4 hours) increases proinflammatory cytokine (IFN-β) level in tumors[1].MSA-2 dimer (60 mg kg; s.c.; 4 hours) concentrations is observed in tumors than in plasma or other nontumor tissues [1].MSA-2 dimer (THP-1 cells) induces phosphorylation of both TBK1 and IR. MSA-2 dimer (10 μM and 33 μM; macrophages) induces IFN-β[1].MSA-2 dimer also exhibits dose-dependent antitumor activity when administered by IT, SC, or PO routes[1]. [1]. Pan BS, et al. An orally available non-nucleotide STING agonist with antitumor activity. Science. 2020;369(6506):eaba6098.