Nocodazole

Catalog No.S2775 Batch:s277501

Print

Technical Data

Formula

C14H11N3O3S
Molecular Weight 301.32 CAS No. 31430-18-9
Solubility (25°C)* In vitro DMSO 7 mg/mL (23.23 mM)
Water Insoluble
Ethanol Insoluble
In vivo (Add solvents to the product individually and in order)
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.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description 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. This compound induces apoptosis.
Targets
Microtubules [2]
(Cell-free assay)		 Abl [1]
(Cell-free assay)		 Abl (E255K) [1]
(Cell-free assay)		 Abl (T315I) [1]
(Cell-free assay)
0.21 μM 0.53 μM 0.64 μM
In vitro

Nocodazole is a high-affinity ligand for the cancer-related kinases including Abl phosphorylated, c-Kit, BRAF, and MEK with Kd of 0.091 μM, 1.6 μM, 1.8 μM and 1.6 μM, respectively. In addition, the Kd 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]

Protocol (from reference)

Cell Assay:

[7]
  • Cell lines

    H1975 cells

  • Concentrations

    50 ng/ml

  • Incubation Time

    24 h

  • Method

    Cells were treated with indicated concentration of this compound for 24 hour.
Animal Study:

[5]
  • Animal Models

    Nude mice with COLO-205 tumor xenografts

  • Dosages

    5 mg/kg

  • Administration

    Administered via i.p.

References

  • 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/

Customer Product Validation

<p>A, HeLa cells were treated with DMSO, Taxol (100 nM for 16 h), or Nocodazole (Noco, 100 ng/ml for 16 h). Total cell lysates were probed with the indicated antibodies against Hippo components on Phos-tag SDS-polyacrylamide gels. O and * mark the non-phosphorylated and phosphorylated proteins, respectively.</p>

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

AURKA and PRL-3

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

(B) HeLa cells were treated with DMSO, Taxol or Nocodazole (Noco). Total cell lysates were probed with the indicated antibodies on Phos-tag or regular SDS-polyacrylamide gels.

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

A and B, SUM159 cells were treated with either DMSO, 20 μm Taxol, or 1 μm nocodazole (Noc) for 1-2 h before fixation. Fixed cells were co-stained for IRS-2 (green) and tubulin (red).

Data from [ , , J Biol Chem, 2017, 292(19):7806-7816 ]

Selleck's Nocodazole Has Been Cited by 136 Publications

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

RETURN POLICY
Selleck Chemical’s Unconditional Return Policy ensures a smooth online shopping experience for our customers. If you are in any way unsatisfied with your purchase, you may return any item(s) within 7 days of receiving it. In the event of product quality issues, either protocol related or product related problems, you may return any item(s) within 365 days from the original purchase date. Please follow the instructions below when returning products.

SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.