Date published: 2026-5-9

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MGA Inhibitors

The term MGA inhibitors refers to a class of chemical compounds designed to target and modulate the activity of MGA (MAX gene-associated) proteins, which play a crucial role in the regulation of various cellular processes. MGA proteins are transcriptional regulators that belong to the b-HLH-LZ (basic Helix-Loop-Helix-Leucine Zipper) family. They are involved in the control of gene expression by acting as transcription factors, binding to specific DNA sequences and influencing the transcription of downstream target genes. MGA proteins are known to interact with other key transcriptional regulators such as MAX and MYC, forming intricate complexes that regulate gene expression networks. These interactions are vital for the maintenance of cellular homeostasis and proper cell growth. MGA inhibitors are designed to modulate the function of MGA proteins by disrupting their interactions with other regulatory molecules or DNA, ultimately affecting the transcriptional activity of the associated target genes.

The development of MGA inhibitors involves a detailed understanding of the molecular interactions and structural characteristics of MGA proteins. Researchers employ computational methods, structural biology, and chemical synthesis to design compounds that can selectively bind to specific regions of MGA proteins, thereby interfering with their normal function. By doing so, these inhibitors have the potential to provide valuable insights into the intricate regulatory networks involving MGA proteins and their associated partners. Additionally, these inhibitors could serve as valuable research tools to dissect the functional roles of MGA in various biological contexts. Overall, the exploration of MGA inhibitors contributes to advancing our understanding of gene regulation and cellular processes, offering potential avenues for further uncovering the complexities of transcriptional control.

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Items 1 to 10 of 12 total

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Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

Imatinib

152459-95-5sc-267106
sc-267106A
sc-267106B
10 mg
100 mg
1 g
$26.00
$119.00
$213.00
27
(1)

Inhibits BCR-ABL kinase by binding to its ATP-binding site, preventing phosphorylation of downstream signaling pathways in chronic myeloid leukemia (CML) cells.

Gefitinib

184475-35-2sc-202166
sc-202166A
sc-202166B
sc-202166C
100 mg
250 mg
1 g
5 g
$63.00
$114.00
$218.00
$349.00
74
(2)

Targets EGFR tyrosine kinase, obstructing ATP binding and suppressing downstream signaling pathways in certain types of lung cancer.

Sorafenib

284461-73-0sc-220125
sc-220125A
sc-220125B
5 mg
50 mg
500 mg
$57.00
$100.00
$250.00
129
(3)

Blocks RAF kinases and VEGFR/PDGFR, hindering cell proliferation and angiogenesis in several cancers.

Dasatinib

302962-49-8sc-358114
sc-358114A
25 mg
1 g
$70.00
$145.00
51
(1)

Inhibits BCR-ABL, SRC family kinases, and other tyrosine kinases, reducing growth and survival of cancer cells in leukemia.

Lapatinib

231277-92-2sc-353658
100 mg
$420.00
32
(1)

Dual inhibitor of EGFR and HER2 kinases, disrupting downstream signaling pathways in HER2-positive breast cancer.

Ruxolitinib

941678-49-5sc-364729
sc-364729A
sc-364729A-CW
5 mg
25 mg
25 mg
$251.00
$500.00
$547.00
16
(1)

Targets JAK1/2 kinases, inhibiting their activity and reducing inflammation and cell proliferation in myeloproliferative neoplasms.

Palbociclib

571190-30-2sc-507366
50 mg
$321.00
(0)

Selectively inhibits CDK4/6, arresting cell cycle progression and suppressing tumor growth in hormone receptor-positive breast cancer.

Vemurafenib

918504-65-1sc-364643
sc-364643A
10 mg
50 mg
$117.00
$423.00
11
(1)

Targets mutated BRAFV600E kinase, disrupting the MAPK signaling pathway and inhibiting growth in melanomas with this mutation.

Ibrutinib

936563-96-1sc-483194
10 mg
$156.00
5
(0)

Irreversibly inhibits BTK kinase, disrupting B-cell receptor signaling and leading to apoptosis in B-cell malignancies like CLL.

CH5424802

1256580-46-7sc-364461
sc-364461A
5 mg
50 mg
$191.00
$902.00
(0)

Specifically inhibits ALK kinase, impeding downstream signaling pathways in ALK-positive non-small cell lung cancer.