Ricolinostat | ACY-1215 | HDAC6 Inhibitor | AmBeed-信号通路专用抑制剂

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产品名称	HD1 ↓ ↑	HD2 ↓ ↑	HDAC ↓ ↑	HDAC1 ↓ ↑	HDAC10 ↓ ↑	HDAC11 ↓ ↑	HDAC2 ↓ ↑	HDAC3 ↓ ↑	HDAC4 ↓ ↑	HDAC5 ↓ ↑	HDAC6 ↓ ↑	HDAC7 ↓ ↑	HDAC8 ↓ ↑	HDAC9 ↓ ↑	其他靶点	纯度
Givinostat HCl monohydrate	++++ HD1-B, IC50: 7.5 nM HD1-A, IC50: 16 nM	+++ HD2, IC50: 10 nM														99%+
MC1568	++ HD1-B (Maize), IC50: 3.4 μM HD1-A (Maize), IC50: 100 nM															96%
Trichostatin A			++++ HDAC, IC50: ~1.8 nM													99%+
Scriptaid			✔													99%+
Valproic acid sodium			✔												Autophagy	97%
AR-42			+++ HDAC, IC50: 30 nM													99%+
Dacinostat			+++ HDAC, IC50: 32 nM													98+%
CUDC-101			++++ HDAC, IC50: 4.4 nM	++++ HDAC1, IC50: 4.5 nM	+++ HDAC10, IC50: 26.1 nM		+++ HDAC2, IC50: 12.6 nM	++++ HDAC3, IC50: 9.1 nM	+++ HDAC4, IC50: 13.2 nM	+++ HDAC5, IC50: 11.4 nM	++++ HDAC6, IC50: 5.1 nM	+ HDAC7, IC50: 373 nM	++ HDAC8, IC50: 79.8 nM	++ HDAC9, IC50: 67.2 nM	EGFR,HER2	99%+
M344			++ HDAC, IC50: 100 nM													99%+
Splitomicin			+ Sir2p, IC50: 60 μM													99%
Panobinostat			++++ HDAC (Reh cells), IC50: 20 nM HDAC (MOLT-4 cells), IC50: 5 nM													98%
Sodium 4-Phenylbutyrate			✔													98%
Vorinostat			+++ HDAC, IC50: ~10 nM													98%
Curcumin			✔												Nrf2,NF-κB	98%
Belinostat			+++ HDAC, IC50: 27 nM													98%
RG-2833				++ HDAC1, Ki: 32 nM				++ HDAC3, Ki: 5 nM								98%
Valproic acid				+ HDAC1, IC50: 0.4 mM												98%
BG45				+ HDAC1, IC50: 2 μM			+ HDAC2, IC50: 2.2 μM	+ HDAC3, IC50: 289 nM								99%+
Entinostat				+ HDAC1, IC50: 0.51 μM				+ HDAC3, IC50: 1.7 μM								98%
Resminostat				+++ HDAC1, IC50: 42.5 nM				++ HDAC3, IC50: 50.1 nM			++ HDAC6, IC50: 71.8 nM					98+%
Romidepsin				+++ HDAC1, IC50: 36 nM			+++ HDAC2, IC50: 47 nM									99%+
Parthenolide				✔											NF-κB,p53	97% HPLC
Tacedinaline				+ HDAC1, IC50: 0.9 μM			+ HDAC2, IC50: 0.9 μM	+ HDAC3, IC50: 1.2 μM								98%
Mocetinostat				++ HDAC1, IC50: 0.15 μM		+ HDAC11, IC50: 0.59 μM	+ HDAC2, IC50: 0.29 μM	+ HDAC3, IC50: 1.66 μM								98%
WT-161				++++ HDAC1, IC50: 8.35 nM			+++ HDAC2, IC50: 15.4 nM				++++ HDAC6, IC50: 0.4 nM					99%+
Fimepinostat				++++ HDAC1, IC50: 1.7 nM	++++ HDAC10, IC50: 2.8 nM	++++ HDAC11, IC50: 5.4 nM	++++ HDAC2, IC50: 5.0 nM	++++ HDAC3, IC50: 1.8 nM			+++ HDAC6, IC50: 27 nM					99%+
Tucidinostat				++ HDAC1, IC50: 95 nM	++ HDAC10, IC50: 78 nM		++ HDAC2, IC50: 160 nM	++ HDAC3, IC50: 67 nM								99%+
Santacruzamate A							++++ HDAC2, IC50: 119 pM									99%+
(E,E)-RGFP966								++ HDAC3, IC50: 80 nM								99%+
LMK-235									+++ HDAC4, IC50: 11.9 nM	++++ HDAC5, IC50: 4.2 nM						99%+
Tasquinimod									✔							99%+
CAY10603											++++ HDAC6, IC50: 2 pM					98%
Tubastatin A											+++ HDAC6, IC50: 15 nM					98%
Tubacin											++++ HDAC6, IC50: 4 nM					99%+
ACY-738											++++ HDAC6, IC50: 1.7 nM					99%+
Nexturastat A											++++ HDAC6, IC50: 5 nM					99%+
BRD73954											+++ HDAC6, IC50: 36 nM		++ HDAC8, IC50: 120 nM			99%
Tubastatin A HCl											+++ HDAC6, IC50: 15 nM		+ HDAC8, IC50: 854 nM			98%
PCI-34051													+++ HDAC8, IC50: 10 nM			99%+
Ricolinostat				++ HDAC1, IC50: 58 nM			++ HDAC2, IC50: 48 nM	++ HDAC3, IC50: 51 nM			++++ HDAC6, IC50: 4.7 nM		++ HDAC8, IC50: 100 nM			99%+
Droxinostat								+ HDAC3, IC50: 16.9 μM			+ HDAC6, IC50: 2.47 μM		+ HDAC8, IC50: 1.46 μM			99%+
Abexinostat				++++ HDAC1, Ki: 7 nM	+++ HDAC10, IC50: 24 nM		+++ HDAC2, Ki: 19 nM	++++ HDAC3/SMRT, Ki: 8.2 nM			+++ HDAC6, Ki: 17 nM		+ HDAC8, IC50: 280 nM			98%+
Citarinostat				+++ HDAC1, IC50: 35 nM			+++ HDAC2, IC50: 45 nM	+++ HDAC3, IC50: 46 nM			++++ HDAC6, IC50: 2.6 nM		++ HDAC8, IC50: 137 nM			99%+
HPOB				+ HDAC1, IC50: 2.9 μM	+ HDAC10, IC50: 3.0 μM		+ HDAC2, IC50: 4.4 μM	+ HDAC3, IC50: 1.7 μM			++ HDAC6, IC50: 56 nM		+ HDAC8, IC50: 2.8 μM			97%
Quisinostat 2HCl				++++ HDAC1, IC50: 0.11 nM	++++ HDAC10, IC50: 0.46 nM	++++ HDAC11, IC50: 0.37 nM	++++ HDAC2, IC50: 0.33 nM	++++ HDAC3, IC50: 4.86 nM	++++ HDAC4, IC50: 0.64 nM	++++ HDAC5, IC50: 3.69 nM			++++ HDAC8, IC50: 4.26 nM			97%
Domatinostat				+ HDAC1, IC50: 1.20 μM	+ HDAC10, IC50: 21 μM	+ HDAC11, IC50: 9.7 μM	+ HDAC2, IC50: 1.12 μM	+ HDAC3, IC50: 0.57 μM		+ HDAC5, IC50: 11.3 μM				+ HDAC9, IC50: 50 μM		99%+
TMP269									++ HDAC4, IC50: 157 nM	++ HDAC5, IC50: 97 nM		+++ HDAC7, IC50: 43 nM		+++ HDAC9, IC50: 23 nM		99%+
Pracinostat				++ HDAC1, IC50: 49 nM	+++ HDAC10, IC50: 40 nM	++ HDAC11, IC50: 93 nM	++ HDAC2, IC50: 96 nM	+++ HDAC3, IC50: 43 nM	++ HDAC4, IC50: 56 nM	+++ HDAC5, IC50: 47 nM	+ HDAC6, IC50: 1.008 μM	++ HDAC7, IC50: 137 nM	++ HDAC8, IC50: 140 nM	++ HDAC9, IC50: 70 nM		99%+
TMP195									++ HDAC4, Ki: 59 nM	++ HDAC5, Ki: 60 nM		+++ HDAC7, Ki: 26 nM		+++ HDAC9, Ki: 15 nM		99%+
1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多，抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用，但抑制强度暂时没有相关数据。

靶点	HDAC8 HDAC8, IC50:100 nM HDAC3 HDAC3, IC50:51 nM HDAC6 HDAC6, IC50:4.7 nM HDAC2 HDAC2, IC50:48 nM HDAC1 HDAC1, IC50:58 nM
描述	There are 18 mammalian HDACs, HDAC 1 - 11 and sirt 1 - 7. One of the member, HDAC6 can target specific substrates like HSP90 andα-tubulin which involve in protein trafficking and degradation or cell shape and migration, thus participates in the pathways relating to neurodegenerative diseases, cancer, and immunology^[1]. ACY-1215, also called Rocilinostat, is a potent and selective HDAC6 inhibitor with IC50 value of 4.7 nM (measured by HDAC enzymatic assays), while exhibits minimal inhibition on HDAC4, HDAC5, HDAC7, HDAC9, HDAC11, Sirtuin1, and Sirtuin2 (IC50 > 1 μM) and slightly inhibits HDAC8 (IC50 = 0.1 μM). A dose-dependent increased acetylatedα-tubulin and no affecting acetylation of histones can be observed in MM.1S cells with treatment of ACY-1215 for 6 hours, which confirming the selective inhibition of ACY-1215 on low dose (0.62 μM). ACY-1215 (0 - 4 μM) in combination with bortezomib (0 - 5 nM) for 24 and 48 hours in MM.1S cells and for 48 hours in RPMI8226 cells induce synergistic anti-MM activity. This may due to ACY-1215 disrupting aggresome formation with increased levels of polyubiquitinated protein, then triggers the apoptosis by the induction of ER stress and UPR. And a significant therapeutic advantage was found by combining ACY-1215 (50 mg/kg, IP) with bortezomib (0.5 mg/kg, IV) compared with either agent alone for 3 weeks, which echoes the synergistic activity cellar study^[2]. ACY-1215 alone/ in combination with dexametrasone and either bortezomib or lenalidomide is currently under phase I, II clinical trials for multiple myeloma^[3].
作用机制	ACY-1215 can monodentate Zn²⁺ of HDAC6 through its phenylhydroxamate structure^[4].

Cell Line MDA-MB-453 MDA-MB-436 HEK-293 cells HT1080 cells HeLa cells OPM-2 cells Human neutrophils Mouse neutrophils Peripheral blood mononuclear cells (PBMCs) PBMCs from NSCLC patients WSU-NHL Hut-78 Jeko-1 MM.1S cells U266 cells CD34+ HSPCs	Concentration	Treated Time	Description	References
MDA-MB-453	2.5 μM	72 h	Induced apoptosis	Nat Cancer. 2023 Feb;4(2):257-275.
MDA-MB-436	2.5 μM	72 h	No significant apoptosis observed	Nat Cancer. 2023 Feb;4(2):257-275.
HEK-293 cells	2.5 µM	24 h	Assess the cytotoxicity of Ricolinostat on HEK-293 cells	Nucleic Acids Res. 2021 Sep 7;49(15):8974-8986.
HT1080 cells	2.5 µM	24 h	Assess the cytotoxicity of Ricolinostat on HT1080 cells	Nucleic Acids Res. 2021 Sep 7;49(15):8974-8986.
HeLa cells	2.5 µM	24 h	Assess the cytotoxicity of Ricolinostat on HeLa cells	Nucleic Acids Res. 2021 Sep 7;49(15):8974-8986.
OPM-2 cells	5 µM and 10 µM	72 h	Similar trends were observed on the MM cell line OPM-2	Leukemia. 2021 Jan;35(1):201-214.
Human neutrophils	10, 2, 0.4, 0.08 µM	1 h	Ricolinostat significantly reduced the release of CitH3 in PMA-treated human neutrophils, indicating its inhibition of NETosis.	iScience. 2021 Oct 11;24(11):103256.
Mouse neutrophils	10, 2, 0.4, 0.08 µM	1 h	Ricolinostat efficiently decreased the release of CitH3 in PMA-treated mouse neutrophils, demonstrating its efficacy in inhibiting NETosis.	iScience. 2021 Oct 11;24(11):103256.
Peripheral blood mononuclear cells (PBMCs)	2.5 μM	24 h	Ricolinostat significantly reduced the proportion of CD4+FOXP3+ Tregs and upregulated the expression of the CD69 activation marker on CD8+ and CD4+ T cells, indicating it promoted T cell activation.	Cancer Discov. 2017 Aug;7(8):852-867.
PBMCs from NSCLC patients	2.5 μM	24 h	Ricolinostat significantly reduced the proportion of Tregs in PBMCs from NSCLC patients and upregulated the expression of the CD69 activation marker on CD8+ and CD4+ T cells, indicating it promoted T cell activation.	Cancer Discov. 2017 Aug;7(8):852-867.
WSU-NHL	0.01–100 µM	24–72 h	Ricolinostat significantly inhibited cell viability with IC50 values ranging from 1.51 to 8.65 µM.	Apoptosis. 2017 Jun;22(6):827-840.
Hut-78	0.01–100 µM	24–72 h	Ricolinostat significantly inhibited cell viability with IC50 value of 1.51 µM.	Apoptosis. 2017 Jun;22(6):827-840.
Jeko-1	0.01–100 µM	24–72 h	Ricolinostat significantly inhibited cell viability with IC50 values ranging from 1.51 to 8.65 µM.	Apoptosis. 2017 Jun;22(6):827-840.
MM.1S cells	5 µM and 10 µM	72 h	In flow cytometry, there was a 2.5-fold (5 µM) and 3.1-fold (10 µM) increase in CD38 expression at 72 h of treatment by mean fluorescence intensity (MFI) ( p<0 . 0 0 0 1 , n=13)	Leukemia. 2021 Jan;35(1):201-214.
U266 cells	1, 5, and 10 µM	48 h	CD38 expression on U266 cells before and after treatment with ricolinostat, ACY-241, and WT-161 at fcs of 1, 5, and 10 µM	Leukemia. 2021 Jan;35(1):201-214.
CD34+ HSPCs	2 μM	7 days	To study the effect of Ricolinostat on the differentiation of CD34+ HSPCs into megakaryocytes, Ricolinostat significantly increased the percentage of CD34+CD41a+ MkPs and CD41a+CD61+ MKs.	Stem Cell Res Ther. 2022 Feb 5;13(1):54.

Species Mice Mouse Mice Mice Mice	Animal Model EL4 lymphoma and LLC lung carcinoma models Endotoxic shock model KP mice (genetically engineered mice with KrasG12D mutation and p53 loss) MDA-MB-453 and MDA-MB-436 xenograft models EGFP-expressing mouse embryos	Administration	Dosage	Frequency	Description	References
Mice	EL4 lymphoma and LLC lung carcinoma models	Intraperitoneal injection	50 mg/kg	Once daily for 10 days	Ricolinostat alone did not significantly affect tumor growth, but in combination with entinostat, it substantially delayed tumor progression.	Cancer Immunol Immunother. 2020 Sep;69(9):1929-1936
Mouse	Endotoxic shock model	Intraperitoneal injection	30 mg/kg	Administered on day 2, day 4, and 3 hours before the endpoint	Ricolinostat significantly reduced NETosis and inflammation in a mouse model of endotoxic shock, improving lung functionality and reducing systemic inflammation.	iScience. 2021 Oct 11;24(11):103256.
Mice	KP mice (genetically engineered mice with KrasG12D mutation and p53 loss)	Intraperitoneal injection	50 mg/kg	Once daily for 7 days	Ricolinostat treatment significantly increased the proportion of tumor-infiltrating CD8+ T cells and decreased the proportion of CD4+Foxp3+ Tregs, while upregulating the CD69 activation marker and IFN-γ secretion, indicating it promoted T cell activation and effector function.	Cancer Discov. 2017 Aug;7(8):852-867.
Mice	MDA-MB-453 and MDA-MB-436 xenograft models	Intraperitoneal injection	50 mg/kg	6 days a week for 1 month	Significant antitumor activity was observed in the MDA-MB-453 model, but no significant effect was observed in the MDA-MB-436 model	Nat Cancer. 2023 Feb;4(2):257-275.
Mice	EGFP-expressing mouse embryos	Embryo culture medium	2.5 µM	24 hours	Evaluate the enhancement of gene editing efficiency in mouse embryos by Ricolinostat	Nucleic Acids Res. 2021 Sep 7;49(15):8974-8986.

CAS号	1316214-52-4
分子式	C₂₄H₂₇N₅O₃
分子量	433.5
SMILES Code	O=C(C1=CN=C(N(C2=CC=CC=C2)C3=CC=CC=C3)N=C1)NCCCCCCC(NO)=O
MDL No.	MFCD22666356

别名	ACY-1215; Rocilinostat; ACY-63
运输	蓝冰
InChI Key	QGZYDVAGYRLSKP-UHFFFAOYSA-N
Pubchem ID	53340666

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HDAC8	HDAC8, IC50:100 nM
HDAC3	HDAC3, IC50:51 nM
HDAC6	HDAC6, IC50:4.7 nM
HDAC2	HDAC2, IC50:48 nM
HDAC1	HDAC1, IC50:58 nM

A-172	10 nM	Growth Inhibition Assay	24/48 h	inhibits cell growth time dependently	26150340
CCL-119		Growth Inhibition Assay	48 h	IC50=1.7 μM	26116270
H9		Growth Inhibition Assay	48 h	IC50=1.2 μM	26116270
Hbl-1		Growth Inhibition Assay	48 h	IC50=1.6 μM	26116270
Hbl-2		Growth Inhibition Assay	48 h	IC50=1.9 μM	26116270
HH		Growth Inhibition Assay	48 h	IC50=2.5 μM	26116270
Jeko-1		Growth Inhibition Assay	48 h	IC50=1.5 μM	26116270
Jvm-2		Growth Inhibition Assay	48 h	IC50=4.0 μM	26116270
LR5	0-8μM	Cell Viability Assay	48 h	decreases MM-cell viability in a dose-dependent manner	22262760
MM.1R	0.25/1μM	Function Assay	18 h	increases acetylated α-tubulin	22262760
MM.1R	0-8μM	Cell Viability Assay	48 h	decreases MM-cell viability in a dose-dependent manner	22262760
MM.1S	0-5μM	Function Assay	6 h	increases acetylated α-tubulin	22262760
MM.1S	0.25/1μM	Function Assay	18 h	increases acetylated α-tubulin	22262760
MM.1S	0-8μM	Cell Viability Assay	48 h	decreases MM-cell viability in a dose-dependent manner	22262760
OCI-Ly1		Growth Inhibition Assay	48 h	IC50=2.4 μM	26116270
OCI-Ly10		Growth Inhibition Assay	48 h	IC50=0.9 μM	26116270
OCI-Ly7		Growth Inhibition Assay	48 h	IC50=1.2 μM	26116270
OPM1	0-8μM	Cell Viability Assay	48 h	decreases MM-cell viability in a dose-dependent manner	22262760
OPM2	0-8μM	Cell Viability Assay	48 h	decreases MM-cell viability in a dose-dependent manner	22262760
Rec-1		Growth Inhibition Assay	48 h	IC50=2.3 μM	26116270
Riva		Growth Inhibition Assay	48 h	IC50=2.2 μM	26116270
RPMI	0-8μM	Cell Viability Assay	48 h	decreases MM-cell viability in a dose-dependent manner	22262760
RPMI8226		Growth Inhibition Assay		IC50=1468 ± 310 nM	26443078
RPMI8226	0.25/1μM	Function Assay	18 h	increases acetylated α-tubulin	22262760
Su-DHL2		Growth Inhibition Assay	48 h	IC50=3.3 μM	26116270
Su-DHL4		Growth Inhibition Assay	48 h	IC50=4.7 μM	26116270
Su-DHL6		Growth Inhibition Assay	48 h	IC50=3.2 μM	26116270
Sup-T1		Growth Inhibition Assay	48 h	IC50=1.6 μM	26116270
U87MG	10 nM	Growth Inhibition Assay	24/48 h	inhibits cell growth time dependently	26150340

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