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Cat. No.	Product Name	Target	Signaling Pathways
T60954	HDAC6-IN-6
	HDAC6-IN-6 (化合物 6a) 是 HDAC6的有效抑制剂，可以穿透血脑屏障，IC50值为0.025 μM。HDAC6-IN-6 对 AChE 和 Aβ1-42自聚集具有有效的抑制活性，IC50值分别为 0.72 和 3.0 μM。HDAC6-IN-6 可促进神经突起生长而没有显著的神经毒性。
T82226	HDAC6-IN-21	HDAC	Chromatin/Epigenetic; DNA Damage/DNA Repair
	HDAC6-IN-21（化合物13）为一种靶向组蛋白去乙酰化酶6（histone deacetylase 6（HDAC6））的不可逆抑制剂。
T82225	HDAC6-IN-24	HDAC	Chromatin/Epigenetic; DNA Damage/DNA Repair
	HDAC6-IN-24（化合物N1）是一种HDAC6抑制剂。
T73043	HDAC6-IN-15
	HDAC6-IN-15 是一种选择性组蛋白脱乙酰酶 6(HDAC6)抑制剂。HDAC6-IN-15 对 HDAC6具有有效的抑制活性，IC50值为 38.2 nM。HDAC6-IN-15 可用于癌症和神经退行性疾病的研究。
T36625	LSD1/HDAC6-IN-1 LSD1/HDAC6-IN-1
	LSD1/HDAC6-IN-1 is an orally active compound that functions as a dual inhibitor, targeting lysine specific demethylase 1 (LSD1) and histone deacetylase 6 (HDAC6). This compound demonstrates promising anti-tumor activity and is particularly valuable for research focused on multiple myeloma (MM) [1].
T74003	HDAC3/6-IN-2
	HDAC3/6-IN-2 (化合物 15) 是一种高效的HDAC6和HDAC3抑制剂，IC50值分别为0.368 μM和0.635 μM。此化合物不仅具备抗肿瘤活性，能够诱导癌细胞凋亡，同时通过降低HDAC6和HDAC3水平，与H3乙酰化和α-微管蛋白的上调有关。
T78768	HDAC6-IN-16	HDAC	Chromatin/Epigenetic; DNA Damage/DNA Repair
	HDAC6-IN-16（compound 5c）是基于Quinazolin-4(3H)-One的一种HDAC6抑制剂，具备抑制肿瘤细胞集落形成的抗癌活性。该化合物能够引发G2期细胞周期阻滞并诱导细胞凋亡(apoptosis)。
T61583	CDK/HDAC-IN-1
	CDK/HDAC-IN-1 exhibits potent inhibitory activity towards CDK2/4/6 and HDAC6, with IC50 values of 60.9 ± 2.9 nM, 276 ± 22.3 nM, 27.2 ± 4.2 nM, and 128.6 ± 0.4 nM, respectively.
T64187	HDAC1/6-IN-1
	HDAC1/6-IN-1 是一种有效的 GLP (IC50: 1.3 nM)、HDAC6 (IC50: 13 nM) 和 HDAC1 (IC50: 89 nM)的多靶点抑制剂。HDAC1/6-IN-1 能在蛋白水平上抑制 H3K9 的甲基化和去乙酰化。HDAC1/6-IN-1 能够将癌细胞的细胞周期阻滞在 G0/G1 期，能够诱导癌细胞凋亡，可阻止癌细胞迁移和入侵。
T37068	NR-160
	NR-160 is an inhibitor of histone deacetylase 6 (HDAC6; IC50= 0.03 μM).1It is selective for HDAC6 over HDAC1, -2, -3, -4, and -8 (IC50s = 5.18, 2.26, 8.48, 55.4, and 14.7 μM, respectively). NR-160 is cytotoxic against a panel of seven cancer cell lines (IC50s = 22.5-51.8 μM). It enhances cytotoxicity induced by bortezomib in HL-60 cells, as well as cytotoxicity induced by epirubicin or daunorubicin in CCRF-HSB-2 T cell acute lymphoblastic leukemia cells.