Date published: 2026-4-24

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hnRNP U Inhibitors

The class of hnRNP U inhibitors is characterized by a diverse set of compounds that modulate various aspects of cellular function to ultimately influence the activity of hnRNP U indirectly. These inhibitors act on multiple fronts, including DNA damage and repair, transcription regulation, mRNA processing, and chromatin remodeling. Given hnRNP U's broad involvement in RNA biology and chromatin structure, compounds such as etoposide exploit the DNA damage response and transcriptional inhibition respectively to modulate hnRNP U indirectly. Etoposide, through its impact on topoisomerase II, triggers DNA damage responses that can sequester hnRNP U away from its normal activities towards damaged sites, affecting its availability for RNA metabolic processes. Similarly, actinomycin D's binding to the transcription initiation complex impedes the transcription machinery, reducing hnRNP U transcription or impacting its regulatory gene targets, leading to decreased hnRNP U functionality.

On another front, the use of spliceosome inhibitors like pladienolide B and meayamycin B highlights the intricacies of RNA splicing as a regulatory mechanism for hnRNP U. By disrupting the splicing of pre-mRNAs, these inhibitors could influence the post-transcriptional regulation activities of hnRNP U. For instance, pladienolide B's binding to the SF3b complex alters splicing dynamics, affecting hnRNP U's role in the splicing of specific transcripts critical for its function. Additionally, the modulation of phosphorylation states and chromatin structure through agents like CX-4945 and MS-275 respectively, demonstrates an indirect approach to alter hnRNP U activity. CX-4945's inhibition of CK2 affects phosphorylation-dependent processes, possibly diminishing hnRNP U's RNA-binding affinity or modulating its interactions with other splicing factors. In contrast, MS-275's impact on histone acetylation levels can change the transcriptional landscape, influencing the expression of genes that hnRNP U regulates or is co-regulated with. Collectively, these hnRNP U inhibitors operate by intricately altering cellular processes that hnRNP U is inherently dependent upon, resulting in the indirect inhibition of its function in RNA processing and chromatin architecture.

SEE ALSO...

Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

Pladienolide B

445493-23-2sc-391691
sc-391691B
sc-391691A
sc-391691C
sc-391691D
sc-391691E
0.5 mg
10 mg
20 mg
50 mg
100 mg
5 mg
$299.00
$5699.00
$11099.00
$25500.00
$66300.00
$2875.00
63
(2)

Pladienolide B is a spliceosome inhibitor that targets the SF3b complex, crucial for pre-mRNA splicing. By disrupting normal splicing, it can indirectly affect hnRNP U function, which is implicated in RNA processing and transport. This disruption could lead to misregulated alternative splicing of pre-mRNAs that are essential for hnRNP U's role in RNA metabolism, ultimately diminishing its functional repertoire within the cell.

Etoposide (VP-16)

33419-42-0sc-3512B
sc-3512
sc-3512A
10 mg
100 mg
500 mg
$51.00
$231.00
$523.00
63
(1)

Etoposide interferes with the action of DNA topoisomerase II, leading to DNA damage and the potential disruption of chromatin remodeling processes. HnRNP U is involved in chromatin organization; thus, etoposide's action can indirectly influence hnRNP U by creating a DNA damage response that shifts hnRNP U's normal functioning towards DNA repair pathways, thereby modulating its availability for regular chromatin and RNA-related processes.

MS-275

209783-80-2sc-279455
sc-279455A
sc-279455B
1 mg
5 mg
25 mg
$24.00
$90.00
$212.00
24
(2)

MS-275 is a histone deacetylase inhibitor, altering chromatin structure and gene expression. By changing the acetylation status of histones, MS-275 can modulate the transcription of genes associated with hnRNP U function or expression, which can indirectly reduce hnRNP U activity in RNA metabolism and chromatin remodeling.

Triptolide

38748-32-2sc-200122
sc-200122A
1 mg
5 mg
$90.00
$204.00
13
(1)

Triptolide is known to inhibit RNA polymerase II activity, thereby suppressing transcription globally. By reducing overall transcriptional output, triptolide can lead to decreased hnRNP U levels, indirectly affecting its role in RNA processing and metabolism.

ICRF-193

21416-68-2sc-200889
sc-200889A
1 mg
5 mg
$341.00
$927.00
7
(1)

ICRF-193 is a DNA topoisomerase II inhibitor that prevents the religation step of the DNA breakage-reunion reaction, resulting in cytotoxic DNA lesions. By causing DNA damage and initiating DNA repair mechanisms, ICRF-193 can indirectly impact hnRNP U, which may be redirected to DNA repair foci, thereby modulating its normal RNA-related functions.

Mitoxantrone

65271-80-9sc-207888
100 mg
$285.00
8
(1)

Mitoxantrone intercalates into DNA and inhibits topoisomerase II, affecting DNA replication and RNA transcription. It can indirectly modulate hnRNP U's activity by changing the transcriptional landscape, including the potential downregulation of genes involved in hnRNP U's functional pathways.

CX-4945

1009820-21-6sc-364475
sc-364475A
2 mg
50 mg
$183.00
$800.00
9
(2)

CX-4945 is a casein kinase 2 (CK2) inhibitor. CK2 phosphorylation is critical for various cellular processes, including RNA processing. Inhibition of CK2 by CX-4945 can indirectly decrease hnRNP U's phosphorylation status, possibly affecting its RNA-binding affinity and, consequently, its function in mRNA processing and transport.

Bortezomib

179324-69-7sc-217785
sc-217785A
2.5 mg
25 mg
$135.00
$1085.00
115
(2)

Bortezomib is a proteasome inhibitor, leading to the accumulation of misfolded proteins and the disruption of normal cellular proteostasis. HnRNP U, being involved in RNA metabolism, could be indirectly inhibited as the proteasome inhibition might alter its turnover rate or the regulatory proteins that control hnRNP U's function.

Flavopiridol Hydrochloride

131740-09-5sc-207687
10 mg
$317.00
(2)

Flavopiridol Hydrochloride is a cyclin-dependent kinase inhibitor that can suppress transcription elongation by inhibiting positive transcription elongation factor b (P-TEFb). This inhibition can indirectly affect hnRNP U function by altering the transcription of genes involved in its regulatory network, potentially reducing hnRNP U's involvement in RNA splicing and metabolism.