annexin a

Timonacic (Thioproline) has been used in trials studying the treatment of HIV Infections.

Hydrocortisone 17-butyrate (Cortisol 17-butyrate) is a synthetic glucocorticoid receptor agonist with antiinflammatory, antipruritic and vasoconstrictive effects.

Dexamethasone acetate (NSC 39471) is the acetate salt form of Dexamethasone, a synthetic adrenal corticosteroid with potent anti-inflammatory properties. In addition to binding to specific nuclear steroid receptors, dexamethasone also interferes with NF-kB activation and apoptotic pathways. This agent lacks the salt-retaining properties of other related adrenal hormones.

Amcinonide (CL-34699) is a Corticosteroid. The mechanism of action of amcinonide is as a Corticosteroid Hormone Receptor Agonist.

LCKLSL acetate is a competitive annexin A2 (AnxA2) inhibitor. LCKLSL acetate potently inhibits the binding of tissue plasminogen activator (tPA) to AnxA2 and the generation of plasmin. LCKLSL acetate has anti-angiogenic roles.

(R)-SL18 is a degrader of ANXA3 that facilitates its breakdown via ubiquitination. This compound can inhibit the proliferation, migration, invasion, and colony formation of breast cancer cells, while also inducing apoptosis. (R)-SL18 is applicable for research in triple-negative breast cancer.

ANXA3 degrader 1 (Compound 18a5) is a highly selective ANXA3 degrader with activity against cancer cells. It demonstrates significant inhibitory effects in a triple-negative breast cancer (TNBC) tumor xenograft model, with a tumor growth inhibition (TGI) rate of 96%.

PY-60 can effectively activate YAP transcriptional activity against annexin A2 (ANXA2) (Kd value of 1.4 µM). PY-60 activates a pro-proliferative, YAP-dependent transcriptional program in adult animals that are able to remodel the epidermis through proliferation.

Hydrocortisone acetate (Cortisol 21-acetate) is the synthetic acetate salt form of hydrocortisone, a corticosteroid with anti-inflammatory and immunosuppressive properties.

LCKLSL hydrochloride is a hexapeptide compound and competitive inhibitor of membrane-bound protein A2 (AnxA2) with potential anti-angiogenic activity that inhibits the development of autoimmune encephalomyelitis (EAE) in mice.

A2ti-1 is a highly selective inhibitor of annexin A2 S100A10 heterotetramer (A2t) (IC50: 24 μM) that inhibits ARV-mediated activation of Src and p38 mitogen-activated protein kinase (MAPK). A2ti-1 can be used to study human papillomavirus type 16 (HPV16) infection.

AS-99 is a first-in-class, potent, and selective ASH1L histone methyltransferase inhibitor (IC50= 0.79 μM, Kd= 0.89 μM) with anti-leukemic activity, blocking cell proliferation, inducing apoptosis and differentiation, downregulating MLL fusion target genes, and reducing the leukemia burden in vivo[1].

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. It blocks cell proliferation, induces apoptosis and differentiation, downregulates MLL fusion target genes, and reduces the leukemia burden in vivo[1].

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.

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.

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......

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.

Ac9-25 TFA, an N-terminal peptide of Annexin I, functions as a formyl peptide receptor (FPR) agonist, activating neutrophil NADPH oxidase via FPR [1] [2].

A11, a cell-penetrating peptide, integrates the HIV-1 Tat protein transduction domain with an 11-amino acid segment from the annexin A1 N-terminus (residues 20-30). This compound disrupts the interaction between annexin A1 and the Eph receptor tyrosine kinase A2 (EphA2), leading to enhanced EphA2 ubiquitination in HK1 nasopharyngeal carcinoma (NPC) cells. At a concentration of 10 µM, A11 curtails proliferation, migration, and invasion of HK1 and 5-8F NPC cells. Furthermore, A11 demonstrably diminishes tumor volume in mouse xenograft models of 5-8F and HK1 NPC in vivo.

Tat-NTS peptide, a cell-penetrating compound, comprises the HIV-1 Tat protein transduction domain fused with a 10-amino acid sequence (residues 228-237) from the repeat III domain of annexin A1, serving as a nuclear translocation signal (NTS). This peptide hinders the interaction between annexin A1 and importin β, obstructing annexin A1's nuclear entry in primary mouse hippocampal neurons. Tat-NTS effectively prevents apoptosis triggered by glucose-oxygen deprivation and reperfusion in these neurons. When administered in vivo at a dosage of 10 mg/kg, it significantly reduces infarct size, minimizes neuronal apoptosis, and improves navigation performance in the Morris water maze test for mice subjected to ischemia-reperfusion injury via middle cerebral artery occlusion (MCAO).

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).

N-Boc-Phe-Leu-Phe-Leu-Phe (Boc-FLFLF) is a formyl peptide receptor 1 (FPR1) antagonist that increases pain effects and inhibits the antinociceptive activity of annexin. Boc-FLFLF is extensively used in FPR research.

Ac2-26, an annexin A1 mimetic peptide, was able to attenuate renal inflammatory injury in a diabetic mouse model through inhibition of p38MAPK/NF-κB, as well as sepsis-induced cardiomyocyte apoptosis through the LXA4/PI3K/AKT signalling pathway, and hepatic ischaemia-reperfusion injury in mice by modulating IL-22/IL-22R1/STAT3 signalling pathway.