annexin a

PY-60 可以有效激活针对膜联蛋白 A2（ANXA2）(Kd值为1.4 µM)的 YAP 转录活性 。 PY-60 在能够通过增殖重塑表皮的成年动物中激活促增殖、依赖于 YAP 的转录程序。

Dexamethasone acetate (NSC 39471) 是一种糖皮质素类甾体，有抗炎和免疫抑制活性。它可研究眼部感染。

Timonacic (Thioproline) 是一种可用于研究急性病和肝脏疾病的佐剂。它能够诱导逆转，也可用于一些癌症病例的研究。

Amcinonide (CL-34699) 是皮质类固醇。它能够抑制NO 从活化的小胶质细胞释放(IC50:3.38 nM)，具有糖皮质激素受体亲和力。 它是皮质类固醇激素受体激动剂。

LCKLSL acetate 是一种竞争性膜联蛋白 A2 (AnxA2) 抑制剂。 LCKLSL acetate 有效抑制组织纤溶酶原激活剂 (tPA) 与 AnxA2 的结合和纤溶酶的产生。 LCKLSL acetate 具有抗血管生成作用。

Hydrocortisone 17-butyrate (Cortisol 17-butyrate) 是一种肾上腺皮质激素类药物。

LCKLSL hydrochloride 是一种六肽化合物，也是竞争性膜联蛋白 A2（AnxA2）抑制剂，具有潜在的抗血管生成活性，抑制小鼠自身免疫性脑脊髓炎（EAE）的发展

ANXA3 degrader 1 (Compound 18a5) 是一种高度选择性的ANXA3降解剂，并具有癌细胞抑制活性。在三阴性乳腺癌 (TNBC) 肿瘤异种移植模型中，ANXA3 degrader 1 显示出显著的抑制效果 (TGI = 96%)。

(R)-SL18 是一种ANXA3降解剂，能够通过泛素化途径降解ANXA3蛋白。它能够抑制乳腺癌细胞的增殖、迁移、侵袭和克隆形成，并诱导细胞凋亡 (apoptosis)，适用于三阴性乳腺癌的研究。

Hydrocortisone acetate (Cortisol 21-acetate) 是皮质类固醇，能够减少轻微皮肤刺激或痔疮引起的肿胀、搔痒和疼痛。

ABO acts as an annexin A7 modulator, specifically binding to Thr286 to inhibit its phosphorylation on threonine (not on serine or tyrosine) residues within human umbilical vein endothelial cells (HUVECs). This compound furthers the annexin A7 interaction with the EF-hand protein GCA, leading to reduced GCA phosphorylation, lowered intracellular calcium levels, and enhanced autophagy in COS-7 cells. Moreover, ABO lessens phosphorylation of the microtubule-associated protein 1 light chain (LC3) in HUVECs and impedes the upregulation of phosphatidylcholine-specific phospholipase C (PC-PLC) due to oxidized low-density lipoprotein in vascular endothelial cells (VECs). In animal models, specifically apoE-/- mice on a Western diet, administration of ABO (50 or 100 mg/kg per day) has been shown to decrease PC-PLC expression, promote autophagy, and reduce apoptosis, lipid accumulation, and the extent of atherosclerotic plaques in the aortic endothelium.

ExcisaninA may be a potent inhibitor of AKT signaling pathway in tumor cells, it can inhibit invasion by suppressing MMP-2 and MMP-9 expression, it may be a potential anti-metastatic chemotherapeutic agent for the treatment of breast cancer. Excisanin A shows comparable inhibitory effects on the LPS-induced production of NO and PGE2, and activation of NF-kappaB without affecting cell viability.Excisanin A induces apoptosis in colon cancer cell line SW620 as determined by Annexin V staining, the cleavage of caspase-3 and the proteolytic degradation of poly (ADP-ribose) polymerase (PARP).

LCKLSL, an N-terminal hexapeptide, acts as a competitive inhibitor of annexin A2 (AnxA2), effectively preventing the binding of tissue plasminogen activator (tPA) to AnxA2 while also inhibiting the generation of plasmin. In addition, LCKLSL exhibits anti-angiogenic properties.

Ac9-25 TFA, 膜联蛋白 I N 端肽，作为甲酰肽受体(FPR)的激动剂，能激活中性粒细胞NADPH氧化酶通过FPR。

MHY219 is a novel HDAC inhibitor. MHY219 induces apoptosis via up-regulation of androgen receptor expression in human prostate cancer cells. MHY219 was shown to enhance the cytotoxicity on DU145 cells (IC50, 0.36 μM) when compared with LNCaP (IC50, 0.97 μM) and PC3 cells (IC50, 5.12 μM). MHY219 showed a potent inhibition of total HDAC activity when compared with SAHA. MHY219 increased histone H3 hyperacetylation and reduced the expression of class I HDACs (1, 2 and 3) in prostate cancer cells. MHY219 effectively increased the sub-G1 fraction of cells through p21 and p27 dependent pathways in DU145 cells. MHY219 significantly induced a G2 M phase arrest in DU145 and PC3 cells and arrested the cell cycle at G0 G1 phase in LNCaP cells. Furthermore, MHY219 effectively increased apoptosis in DU145 and LNCaP cells, but not PC3 cells, according to Annexin V PI staining and Western blot analysis. These results indicate that MHY219 is a potent HDAC inhibitor that targets regulating mu......

N-Boc-Phe-Leu-Phe-Leu-Phe (Boc-FLFLF) 是甲酰肽受体 1(FPR1)拮抗剂，能够增加疼痛作用，抑制膜联蛋白的抗疼痛活性。

AZ-Tak1 is a potent and a relatively selective inhibitor of TAK1 kinase activity, with an IC50 of 0.009 mM. AZ-Tak1 treatment decreased the level of p38 and ERK in mantle cell lymphoma cells, and induced apoptosis in a dose and time dependent manner, with an IC50 of 0.1–0.5 mM. Using the annexin-V and PI staining and FACS analysis, After 48 hours of incubation, AZ-Tak1 (0.1 mM) induced apoptosis in 28%, 34% and 86% of Mino, SP53, and Jeko cells, respectively, which was increased to 32%, 42%, and 86% when 0.5 mM concentration was used.

A11是一种细胞穿透肽，由HIV-1 Tat蛋白质转导域与对应于脂联素A1 N末端第20至30残基的11氨基酸肽连接而成。它减少脂联素A1与Eph受体酪氨酸激酶A2(EphA2)的结合，并在HK1鼻咽癌(NPC)细胞中增加EphA2的泛素化。A11（10 µM）抑制HK1和5-8F NPC细胞的增殖、迁移和侵袭。在体内，A11减少5-8F和HK1 NPC小鼠异种移植模型中的肿瘤体积。

AS-99 TFA is a first-in-class, potent and selective ASH1L histone methyltransferase inhibitor (IC50= 0.79 μM, Kd= 0.89 μM) with anti-leukemic activity. AS-99 TFA blocks cell proliferation, induces apoptosis and differentiation, downregulates MLL fusion target genes, and reduces the leukemia burden in vivo[1]. AS-99 TFA is tested against a panel of 20 histone methyltransferases, including NSD1, NSD2, NSD3, and SETD2. NO significant inhibition is observed at 50 μM of AS-99 TFA on any of the tested histone methyltransferases, indicating over 100-fold selectivity towards ASH1L[1].AS-99 TFA shows effect on the growth of the MLL leukemia cells (MV4;11, MOLM13, KOPN8, RS4;11) with the GI50 values ranging from 1.8 μM to 3.6 μM[1].AS-99 (1-8 μM; 7 days) TFA also induces apoptosis in the MLL leukemia cells, but not in the K562 cells, as assessed by the quantification of the Annexin V positive cells[1].AS-99 TFA suppresses MLL fusion driven transcriptional programs[1]. AS-99 (30 mg kg; i.p.; q.d., treated for 14 consecutive days) TFA reduces leukemia burden in mice[1].AS-99 TFA is used for in vivo studies in mice, which reveals favorable exposure in plasma upon i.v. and i.p. administration (AUC = 9701 hr* ng mL and 10,699 hr* ng mL, respectively), suitable half-life (~5-6 h) and Cmax >10 μM[1]. [1]. David S. Rogawski, Jing Deng, Hao Li, Tomasz Cierpicki, Jolanta Grembecka, et al. Discovery of first-in-class inhibitors of ASH1L histone methyltransferase with anti-leukemic activity. Nat Commun. 2021 May 14;12(1):2792.

A2ti-1 是一种具有高选择性的附件蛋白 A2 S100A10 杂四聚体（A2t）抑制剂（IC50 ： 24 μM）， 抑制ARV介导的Src和p38丝裂原活化蛋白激酶（MAPK）的激活。A2ti-1 可用于研究人类乳头瘤病毒 16 型（HPV16）感染。

Tat-NTS肽是一种能穿透细胞的肽，由HIV-1 Tat蛋白的转导域与对应于脂联素A1重复III域残基228-237的10个氨基酸肽链接而成，扮演核转运信号（NTS）的角色。它通过阻断脂联素A1与进口素β之间的蛋白质-蛋白质相互作用，阻止脂联素A1在初级鼠海马神经元中的核内转运。Tat-NTS抑制初级鼠海马神经元在葡萄糖-氧剥夺及再灌注诱导的细胞凋亡。在体内，Tat-NTS（10 mg/kg）有效减少了由中脑动脉闭塞（MCAO）引起的缺血-再灌注损伤模型小鼠的梗塞体积和神经元凋亡，并缩短了在Morris水迷宫测试中达到平台的时间。

N-terminal peptide of Annexin I (AI/Lipocortin I) that inhibits leukocyte extravasation. Acts as a formyl peptide receptor 1 (FPR1) ligand and stimulates neutrophil NADPH oxidase activation.

CDKI-83 is a potent CDK9 inhibitor. The compound shows effective anti-proliferative activity in human tumour cell lines with GI50 <1 μM, and is capable of inducing apoptosis in A2780 human ovarian cancer cells as determined by the activated caspase-3, Annexin V PI double staining and accumulated cells at the sub-G1 phase of cellcycle. The research results suggest that combined inhibition of CDK9 and CDK1 may result in the effective induction of apoptosis and CDKI-83 has the potential to be developed as an anti-cancer agent.