Nocodazole

製品コードS2775 バッチS277503

印刷

化学情報

Synonyms

R17934, Oncodazole, NSC238159

Storage
(From the date of receipt)

3 years -20°C powder
1 years -80°C in solvent

化学式

C₁₄H₁₁N₃O₃S

分子量

301.32

CAS No.

31430-18-9

Solubility (25°C)*

体外

DMSO

6 mg/mL (19.91 mM)

Water

Insoluble

Ethanol

Insoluble

体内（毎回新しく調製した物を用意してください）

Homogeneous suspension

CMC-NA

≥5mg/ml

Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.

* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

溶剤液（一定の濃度）を調合する

生物活性

製品説明	Nocodazole is a rapidly-reversible inhibitor of microtubule polymerization, also inhibits Abl, Abl(E255K) and Abl(T315I) with IC50 of 0.21 μM, 0.53 μM and 0.64 μM in cell-free assays, respectively. Nocodazole induces apoptosis.
in vitro	Nocodazole is a high-affinity ligand for the cancer-related kinases including Abl phosphorylated, c-Kit, BRAF, and MEK with K_d of 0.091 μM, 1.6 μM, 1.8 μM and 1.6 μM, respectively. In addition, the K_d of this compound for Abl(E255K) phosphorylated, Abl(T315I) phosphorylated, BRAF(V600E) and PI3Kγ is 0.12 μM, 0.17 μM, 1.1 μM and 1.5 μM, respectively. It induces apoptosis in chronic lymphocytic leukemia cells. This chemical inhibits insulin-stimulated glucose transport. It decreases apoptosis in some human colon carcinoma cells. It impairs the morphology and directionality of migrating medial gan-glionic eminence cells. ^[1] At high concentrations, this compound rapidly depolymerizes microtubules in cells, while low concentrations of it inhibit microtubule dynamic instability. ^[2] Mitotic cells incubated with different concentrations are inhibited from progressing to G₁ phase 6 hours after release from the Nocodazole block, with a median inhibitory concentration of 4 nM. Nocodazole-pretreated cells exposed in the absence of this chemical only form free-floating microtubules, whereas pretreated cells exposed in the presence of it-assembled centrosome organize microtubules. ^[3] It disrupts microtubules by binding to β-tubulin. This compound prevents the formation of one of the two interchain disulfide linkages. It impairs the transport of vesicles. It suppress METH-induced cell death and lysosomal dysfunction. METH-induced cell death is significantly decreased by this compound pretreatment in comparison to METH alone. ^[4] It doubles HDR efficiency to up to 30% in iPSCs. It improves the CRISPR-mediated HDR efficiency and has an additive effect on enhancing precise genome editing^[6].
in vivo	The tumor volume and tumor weight of the mice treated with Nocodazole are significantly reduced as compared with those treated with this compound alone. Combined treatment with this chemical strongly enhances apoptosis of COLO 205 tumor xenografts treated with it alone. ^[5]

製品説明

Nocodazole is a rapidly-reversible inhibitor of microtubule polymerization, also inhibits Abl, Abl(E255K) and Abl(T315I) with IC50 of 0.21 μM, 0.53 μM and 0.64 μM in cell-free assays, respectively. Nocodazole induces apoptosis.

in vitro

Nocodazole is a high-affinity ligand for the cancer-related kinases including Abl phosphorylated, c-Kit, BRAF, and MEK with K_d of 0.091 μM, 1.6 μM, 1.8 μM and 1.6 μM, respectively. In addition, the K_d of this compound for Abl(E255K) phosphorylated, Abl(T315I) phosphorylated, BRAF(V600E) and PI3Kγ is 0.12 μM, 0.17 μM, 1.1 μM and 1.5 μM, respectively. It induces apoptosis in chronic lymphocytic leukemia cells. This chemical inhibits insulin-stimulated glucose transport. It decreases apoptosis in some human colon carcinoma cells. It impairs the morphology and directionality of migrating medial gan-glionic eminence cells. ^[1]

At high concentrations, this compound rapidly depolymerizes microtubules in cells, while low concentrations of it inhibit microtubule dynamic instability. ^[2]

Mitotic cells incubated with different concentrations are inhibited from progressing to G₁ phase 6 hours after release from the Nocodazole block, with a median inhibitory concentration of 4 nM. Nocodazole-pretreated cells exposed in the absence of this chemical only form free-floating microtubules, whereas pretreated cells exposed in the presence of it-assembled centrosome organize microtubules. ^[3]

It disrupts microtubules by binding to β-tubulin. This compound prevents the formation of one of the two interchain disulfide linkages. It impairs the transport of vesicles. It suppress METH-induced cell death and lysosomal dysfunction. METH-induced cell death is significantly decreased by this compound pretreatment in comparison to METH alone. ^[4]

It doubles HDR efficiency to up to 30% in iPSCs. It improves the CRISPR-mediated HDR efficiency and has an additive effect on enhancing precise genome editing^[6].

in vivo

The tumor volume and tumor weight of the mice treated with Nocodazole are significantly reduced as compared with those treated with this compound alone. Combined treatment with this chemical strongly enhances apoptosis of COLO 205 tumor xenografts treated with it alone. ^[5]

プロトコル(参考用のみ)

細胞アッセイ	細胞株	H1975 cells
	濃度	50 ng/ml
	反応時間	24 h
	実験の流れ	Cells were treated with indicated concentration of this compound for 24 hour.
動物実験	動物モデル	Nude mice with COLO-205 tumor xenografts
	投薬量	5 mg/kg
	投与方法	Administered via i.p.

参考

https://pubmed.ncbi.nlm.nih.gov/22002881/
http://onlinelibrary.wiley.com/doi/10.1002/ddr.10023/abstract
https://pubmed.ncbi.nlm.nih.gov/7913875/

https://pubmed.ncbi.nlm.nih.gov/22613348/
https://pubmed.ncbi.nlm.nih.gov/12203371/
https://pubmed.ncbi.nlm.nih.gov/28219395/
https://pubmed.ncbi.nlm.nih.gov/34388376/

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カスタマーフィードバック

: , , J Biol Chem, 2016, 291:14761-14772.

: Data from [Data independently produced by , , Cancer Res, 2018, doi:10.1158/0008-5472.CAN-18-0520]

: Data from [Data independently produced by , , Cell Signal, 2016, 28(12):1826-1832]

Selleckの高級品が、幾つかの出版された研究調査結果（以下を含む）で使われた：

The cAMP-PKA signaling initiates mitosis by phosphorylating Bora [ Nat Commun, 2025, 16(1):7898]	PubMed: 40849432
A chromatin-remodeling-independent role for ATRX in protecting centromeric cohesion [ EMBO J, 2025, 44(14):4037-4064]	PubMed: 40437074
EHMT2-mediated R-loop formation promotes the malignant progression of prostate cancer via activating Aurora B [ Clin Transl Med, 2025, 15(1):e70164]	PubMed: 39763034
FTO inhibition enhances the therapeutic index of radiation therapy in head and neck cancer [ JCI Insight, 2025, 10(11)e184968]	PubMed: 40485587
SHCBP1 drives tumor progression in triple-negative breast cancer [ Front Oncol, 2025, 15:1587236]	PubMed: 40799237
Microtubule-dependent regulation of TMEM16A-mediated Ca2+-activated Cl- currents in vascular smooth muscle cells [ J Pharmacol Sci, 2025, 159(3):202-207]	PubMed: 40983463
PLK1 Inhibition Induces Synthetic Lethality in Fanconi Anemia Pathway-Deficient Acute Myeloid Leukemia [ Cancer Res Commun, 2025, 5(4):648-667]	PubMed: 40111122
Synergistic induction of mitotic pyroptosis and tumor remission by inhibiting proteasome and WEE family kinases [ Signal Transduct Target Ther, 2024, 9(1):181.]	PubMed: 38992067
mTORC2-driven chromatin cGAS mediates chemoresistance through epigenetic reprogramming in colorectal cancer [ Nat Cell Biol, 2024, 10.1038/s41556-024-01473-0]	PubMed: 39080411
A noncoding variant confers pancreatic differentiation defect and contributes to diabetes susceptibility by recruiting RXRA [ Nat Commun, 2024, 15(1):9771]	PubMed: 39532884

長期の保管のために-20°Cの下で製品を保ってください。

人間や獣医の診断であるか治療的な使用のためにでない。

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