Date published: 2025-12-20

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C17orf55 Inhibitors

Chemical inhibitors of C17orf55 disrupt the protein's function by targeting various aspects of the cell division cycle, particularly microtubule dynamics and spindle apparatus formation. Paclitaxel and vinblastine interfere with microtubule function, which is an integral part of cell division. Paclitaxel achieves this by stabilizing microtubules, preventing their disassembly and thus hindering the formation of the mitotic spindle. Vinblastine, on the other hand, binds to tubulin, the building block of microtubules, and inhibits their assembly. This action results in the inhibition of mitotic spindle function, which is necessary for successful cell division. Similarly, colchicine and podophyllotoxin target tubulin, with colchicine binding to tubulin and inhibiting polymerization, thereby preventing microtubule formation, while podophyllotoxin prevents the polymerization of tubulin as well, disrupting the formation of microtubules.

Monastrol and S-Trityl-L-cysteine focus on the inhibition of the kinesin Eg5, a motor protein that is essential for the separation of centrosomes and the bipolar spindle formation. Monastrol specifically inhibits the function of Eg5, leading to the formation of monopolar spindles, which are ineffective in cell division. S-Trityl-L-cysteine also inhibits Eg5, reinforcing the inhibition of the mitotic spindle apparatus. Nocodazole contributes to this disruption by depolymerizing microtubules, leading to the disintegration of the microtubule network essential for mitosis. Alisertib, ZM 447439, and BI 2536 take a slightly different approach by inhibiting essential kinases involved in cell cycle progression. Alisertib inhibits Aurora A kinase, which is crucial for mitotic entry and spindle assembly, while ZM 447439 inhibits Aurora kinase, affecting cytokinesis and chromosome alignment. BI 2536 inhibits polo-like kinase 1 (PLK1), which affects spindle formation and checkpoint regulation. Purvalanol A targets cyclin-dependent kinases that are essential for the progression of the cell cycle. By inhibiting these kinases, Purvalanol A halts the cell cycle. Lastly, SP600125 inhibits the Jun N-terminal kinase (JNK), which impacts cell cycle progression and the cell's ability to undergo division, thus indirectly affecting the role of C17orf55 in these processes. Each of these chemical inhibitors, through their unique mechanisms, can disrupt the normal functioning of C17orf55, which plays a role in cell cycle progression and mitosis.

Items 1 to 10 of 12 total

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Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

Taxol

33069-62-4sc-201439D
sc-201439
sc-201439A
sc-201439E
sc-201439B
sc-201439C
1 mg
5 mg
25 mg
100 mg
250 mg
1 g
$40.00
$73.00
$217.00
$242.00
$724.00
$1196.00
39
(2)

Paclitaxel stabilizes microtubules and thereby inhibits their disassembly, which is essential for mitotic spindle formation. C17orf55 is known to be involved in cell cycle progression; stabilization of microtubules can inhibit the function of C17orf55 by preventing proper spindle assembly and cell cycle progression.

Vinblastine

865-21-4sc-491749
sc-491749A
sc-491749B
sc-491749C
sc-491749D
10 mg
50 mg
100 mg
500 mg
1 g
$100.00
$230.00
$450.00
$1715.00
$2900.00
4
(0)

Vinblastine binds to tubulin and inhibits microtubule formation, which is crucial for mitotic spindle function. As C17orf55 has a role in the cell cycle, the disruption of microtubule dynamics by vinblastine will hinder the protein's associated cellular processes.

Colchicine

64-86-8sc-203005
sc-203005A
sc-203005B
sc-203005C
sc-203005D
sc-203005E
1 g
5 g
50 g
100 g
500 g
1 kg
$98.00
$315.00
$2244.00
$4396.00
$17850.00
$34068.00
3
(2)

Colchicine binds to tubulin and inhibits microtubule polymerization, which affects cell division. The inhibition of microtubule dynamics can lead to a functional inhibition of C17orf55 by disrupting cellular processes such as cytokinesis, where C17orf55 is implicated.

Podophyllotoxin

518-28-5sc-204853
100 mg
$82.00
1
(1)

Podophyllotoxin inhibits the polymerization of tubulin, thereby preventing the formation of microtubules. This action interrupts cell division and directly inhibits the cellular functions where C17orf55 is involved, especially mitotic activities.

Monastrol

254753-54-3sc-202710
sc-202710A
1 mg
5 mg
$120.00
$233.00
10
(1)

Monastrol is a kinesin Eg5 inhibitor that disrupts the formation of the bipolar spindle apparatus necessary for mitosis. By disrupting the mitotic spindle, Monastrol functionally inhibits C17orf55 by interfering with the cell cycle processes it is associated with.

Nocodazole

31430-18-9sc-3518B
sc-3518
sc-3518C
sc-3518A
5 mg
10 mg
25 mg
50 mg
$58.00
$83.00
$140.00
$242.00
38
(2)

Nocodazole disrupts microtubule networks by depolymerization and impedes mitotic spindle formation. This impairs the cell division cycle, thus functionally inhibiting the cellular processes that involve C17orf55.

BI 2536

755038-02-9sc-364431
sc-364431A
5 mg
50 mg
$148.00
$515.00
8
(1)

BI 2536 is a polo-like kinase 1 (PLK1) inhibitor, affecting spindle formation and checkpoint regulation. Since C17orf55 is involved in cell cycle regulation, inhibiting PLK1 disrupts the pathway and thereby inhibits C17orf55 functions related to cell cycle progression.

ZM-447439

331771-20-1sc-200696
sc-200696A
1 mg
10 mg
$150.00
$349.00
15
(1)

ZM 447439 is an Aurora kinase inhibitor, which affects cytokinesis and chromosomal alignment. This inhibition impacts the cell cycle and mitotic processes where C17orf55 is known to operate, functionally inhibiting its role.

Purvalanol A

212844-53-6sc-224244
sc-224244A
1 mg
5 mg
$71.00
$291.00
4
(2)

Purvalanol A is a cyclin-dependent kinase inhibitor, which halts cell cycle progression. C17orf55, associated with cell cycle regulation, is functionally inhibited by the disruption of CDK activities, which are crucial for the cell division process.

S-Trityl-L-cysteine

2799-07-7sc-202799
sc-202799A
1 g
5 g
$31.00
$65.00
6
(1)

S-Trityl-L-cysteine is a selective inhibitor of Eg5, which is essential for the formation of mitotic spindles. By inhibiting Eg5, it disrupts spindle assembly, which in turn inhibits the function of C17orf55 in cell cycle regulation.