g-15

G15 是一种高亲和力的、选择性的 G 蛋白偶联雌激素受体(GPER GPR30)拮抗剂(Ki:20 nM)。

AG-1557 hydrochloride (189290-58-2(free base)) 是一种表皮生长因子受体 (EGFR) 酪氨酸激酶抑制剂 (pIC50: 8.194)。

YXG-158（Compound 23-h）是具有口服活性的AR降解剂和CYP17A1抑制剂。该化合物的AR降解活性表现在其DC50值为1.28 μM，而对CYP17A1的抑制作用则体现在其IC50值为100 nM。YXG-158适用于研究恩杂鲁胺耐药性前列腺癌。

[Arg-15,-20,-21,Leu17]-PACAP-Gly-Lys-Arg-NH2 (BM-PACAP) 为合成PACAP 1-27 类似物，展现出明显的松弛效应。

Tezepelumab (AMG 157) 是一种人源化靶向 TSLP 的单克隆抗体 (IgG2λ)，阻止TSLP 与其异二聚体受体相互作用。Tezepelumab 可用于研究晚期哮喘疾病。

Medifoxamine (LG 152) 是一种选择性非单胺氧化酶抑制剂,通过对5 HT 再摄取的抑制展现其抗抑郁活性。Medifoxamine 优先抑制多巴胺再摄取 (dopamine reuptake)。

Sembragiline (EVT-302) 是一种具有选择性的 MAO-B 抑制剂，可用于研究阿尔茨海默病（AD）。

20-HETE Intermediate 15 是20-羟基二十碳四烯酸的中间体。

Cross-linked dextran G 15是一种亲水性凝胶，用于作为凝胶过滤填料。（球型蛋白分离范围：>1500 Da；多糖类分离范围：>1500 Da）。

G150 是高选择性h-cGAS 抑制剂，IC50值为 10.2 nM，用于抑制 dsDNA 引发的干扰素表达。

HO-PEG15-OH is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

Amino-PEG15-amine is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

Azido-PEG15-azide is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

Azido-PEG15-t-butyl ester is a polyethylene glycol (PEG) derived linker, specifically designed for the synthesis of proteolysis-targeting chimeras (PROTACs)[1].

Bis-PEG15-acid is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

Boc-NH-PEG15-azide is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

Boc-NH-PEG15-NH2 is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

Cbz-N-PEG15-amine is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

Fmoc-NH-PEG15-CH2CH2COOH is a PEG-based PROTAC linker utilized for PROTAC synthesis[1].

m-PEG15-alcohol is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

m-PEG15-NHS ester is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

AG1557 (AG-1557) 是一种表皮生长因子受体(EGFR) 酪氨酸激酶抑制剂，pIC50值为 8.194。

PD153035 is a ATP-competitive EGFR inhibitor with an IC50 and Ki of 25 and 6 pM. PD153035 effectively blocks the enhancement of mitogenesis, induction of early gene expression, and oncogenic transformation that occur in response to EGF receptor stimulation. With human fibroblasts and epidermoid carcinoma cells, PD153035 at nanomolar concentrations rapidly inhibits EGFR autophosphorylation. With breast and ovarian cancer cells, PD153035 not only blocks cell growth via inhibition of EGFR, but also upregulates the expression of the tumor suppressor retinoic acid receptor-beta 2 (RAR-beta2).

YM-543, also known as ASP-543, is a selective SGLT2 inhibitor. Sodium-glucose cotransporter 2 (SGLT2) is a specifically expressed transporter in the kidney that plays an important role in renal glucose reabsorption, and its inhibition may present a novel therapeutic strategy for treating diabetes. YM543 potently and selectively inhibited mouse and human SGLT2 activities at nanomolar ranges. In vivo single oral administration of YM543 dose-dependently and significantly reduced blood glucose levels and improved glucose tolerance with a concomitant increase in urinary glucose excretion in KK Ay type 2 diabetic mice, effects that were sustained even after 12 h.