Date published: 2025-9-9

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INS-IGF2 Inhibitors

INS-IGF2 inhibitors are a class of compounds designed to specifically target the interaction between insulin (INS) and insulin-like growth factor 2 (IGF2). Both INS and IGF2 are part of the insulin family of peptides that play critical roles in regulating metabolic and growth-related processes in cells. IGF2 shares structural similarity with insulin and binds to both the insulin receptor and the IGF2 receptor, resulting in the modulation of various signaling pathways that control growth, proliferation, and glucose metabolism. INS-IGF2 inhibitors are engineered to disrupt the binding and signaling interactions between these two molecules, providing insights into how their crosstalk influences cellular functions. By interfering with the INS-IGF2 axis, these inhibitors help delineate the distinct and overlapping roles of insulin and IGF2 in biological systems.

The design of INS-IGF2 inhibitors focuses on selectively targeting the binding interfaces or key regions where insulin and IGF2 interact with their receptors. These inhibitors may mimic the binding sites of either peptide or interfere with receptor-ligand interactions, thus blocking the downstream signaling events. The molecular interactions involved in the inhibition typically include hydrogen bonding, hydrophobic interactions, and electrostatic forces, ensuring that the inhibitors maintain high specificity for disrupting INS-IGF2 signaling. The use of these inhibitors allows researchers to explore the regulatory mechanisms of insulin and IGF2 in various metabolic and growth pathways, shedding light on their individual and combined effects on cellular physiology. By modulating the interplay between insulin and IGF2, INS-IGF2 inhibitors contribute to a deeper understanding of how these two molecules coordinate to regulate critical processes such as cell growth, differentiation, and metabolic homeostasis.

SEE ALSO...

Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

Actinomycin D

50-76-0sc-200906
sc-200906A
sc-200906B
sc-200906C
sc-200906D
5 mg
25 mg
100 mg
1 g
10 g
$73.00
$238.00
$717.00
$2522.00
$21420.00
53
(3)

Actinomycin D may inhibit INS-IGF2 readthrough expression by interfering with RNA polymerase activity, leading to decreased transcription.

Cycloheximide

66-81-9sc-3508B
sc-3508
sc-3508A
100 mg
1 g
5 g
$40.00
$82.00
$256.00
127
(5)

Cycloheximide could inhibit INS-IGF2 readthrough expression by blocking protein synthesis, thereby preventing the translation of mRNA.

Puromycin dihydrochloride

58-58-2sc-108071
sc-108071B
sc-108071C
sc-108071A
25 mg
250 mg
1 g
50 mg
$40.00
$210.00
$816.00
$65.00
394
(15)

Puromycin might inhibit INS-IGF2 readthrough expression by prematurely terminating protein synthesis, leading to the degradation of mRNA.

Anisomycin

22862-76-6sc-3524
sc-3524A
5 mg
50 mg
$97.00
$254.00
36
(2)

Anisomycin may inhibit INS-IGF2 readthrough expression by blocking protein synthesis, thus preventing the translation of mRNA.

Rifampicin

13292-46-1sc-200910
sc-200910A
sc-200910B
sc-200910C
1 g
5 g
100 g
250 g
$95.00
$322.00
$663.00
$1438.00
6
(1)

Rifampicin might inhibit INS-IGF2 readthrough expression by targeting RNA polymerase, leading to decreased transcription of the mRNA.

α-Amanitin

23109-05-9sc-202440
sc-202440A
1 mg
5 mg
$260.00
$1029.00
26
(2)

Alpha-Amanitin may inhibit INS-IGF2 readthrough expression by blocking RNA polymerase II activity, preventing mRNA transcription.

Emetine

483-18-1sc-470668
sc-470668A
sc-470668B
sc-470668C
1 mg
10 mg
50 mg
100 mg
$352.00
$566.00
$1331.00
$2453.00
(0)

Emetine could inhibit INS-IGF2 readthrough expression by blocking protein synthesis, leading to degradation of partially translated mRNA.

Tunicamycin

11089-65-9sc-3506A
sc-3506
5 mg
10 mg
$169.00
$299.00
66
(3)

Tunicamycin might inhibit INS-IGF2 readthrough expression by interfering with protein glycosylation, affecting mRNA translation and stability.

Blasticidin S Hydrochloride

3513-03-9sc-204655A
sc-204655
25 mg
100 mg
$360.00
$475.00
20
(2)

Blasticidin S could inhibit INS-IGF2 readthrough expression by causing premature termination of protein synthesis, leading to mRNA degradation.