Date published: 2026-5-16

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DCAF16 Inhibitors

DCAF16 inhibitors comprise a specialized category of chemical compounds designed to selectively interfere with the function of the DCAF16 protein, a substrate receptor subunit of the CUL4-RING E3 ubiquitin ligase complex. The biological role of DCAF16 involves the recognition and binding of specific protein substrates for ubiquitination, a post-translational modification that typically targets proteins for degradation by the 26S proteasome. By inhibiting DCAF16, these compounds effectively disrupt the ubiquitination and subsequent degradation of substrates, leading to an accumulation of these proteins within the cell. The precise molecular architecture of DCAF16 inhibitors allows them to bind selectively to DCAF16, thereby preventing its interaction with the CUL4-RING E3 ligase complex. This action impedes the transfer of ubiquitin from the E2 enzyme to the substrate, stalling the ubiquitination process. The specificity of DCAF16 inhibitors lies in their ability to target the protein-protein interaction interface between DCAF16 and its substrates, or they may alternatively act by allosterically modulating the conformation of DCAF16, thus reducing its affinity for substrate proteins.

The development of DCAF16 inhibitors is grounded in the understanding of the protein's structure and its role in the ubiquitin-proteasome system. Inhibition of DCAF16 can lead to the stabilization of its substrates, which may be key regulatory proteins involved in various cellular processes, such as cell cycle progression, DNA repair, and signal transduction. The molecular design of these inhibitors ensures they possess high affinity and selectivity for DCAF16, with minimal off-target effects on other proteins. The specificity of these inhibitors is also critical for their ability to modulate the levels of DCAF16 substrates without affecting the global ubiquitin-proteasome system. By focusing on the unique functional domains of DCAF16, researchers aim to create inhibitors that are both effective in their action and limited in their scope, ensuring that the broader cellular proteostasis is maintained. This precise mode of action is pivotal to the utility of DCAF16 inhibitors as research tools to dissect the biological pathways in which DCAF16 is involved and to elucidate the functional consequences of inhibiting this protein within the cell.

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Items 1 to 10 of 12 total

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Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

Rapamycin

53123-88-9sc-3504
sc-3504A
sc-3504B
1 mg
5 mg
25 mg
$63.00
$158.00
$326.00
233
(4)

Rapamycin binds to FKBP12 and together the complex inhibits mTORC1, which can lead to a decrease in protein synthesis. Since DCAF16 is a substrate receptor for CUL4-DDB1 ubiquitin ligase complex, potentially involved in proteasomal degradation, a reduction in protein synthesis could indirectly decrease the functional activity of DCAF16 due to less substrate availability for degradation.

MG-132 [Z-Leu- Leu-Leu-CHO]

133407-82-6sc-201270
sc-201270A
sc-201270B
5 mg
25 mg
100 mg
$60.00
$265.00
$1000.00
163
(3)

MG132 is a proteasome inhibitor that prevents the degradation of ubiquitinated proteins, which could lead to the accumulation of proteins targeted by the DCAF16 complex, thereby functionally inhibiting DCAF16 by overwhelming the degradation system it supports.

Bortezomib

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

Bortezomib is another proteasome inhibitor that could similarly inhibit the function of DCAF16 by preventing the degradation of its substrate proteins, effectively blocking the proteasome pathway in which DCAF16 is involved.

Chloroquine

54-05-7sc-507304
250 mg
$69.00
2
(0)

Chloroquine raises the pH in intracellular vesicles, impairing the process of protein degradation in lysosomes. Since DCAF16 could be involved in lysosome-mediated degradation pathways, chloroquine could inhibit DCAF16 function by disrupting these pathways.

LY 294002

154447-36-6sc-201426
sc-201426A
5 mg
25 mg
$123.00
$400.00
148
(1)

LY294002 is a PI3K inhibitor that can lead to downregulation of the Akt/mTOR pathway. Since this pathway is involved in the regulation of protein synthesis and degradation, inhibiting PI3K could indirectly affect the functional activity of DCAF16 by altering the balance of protein synthesis and degradation.

Autophagy Inhibitor, 3-MA

5142-23-4sc-205596
sc-205596A
50 mg
500 mg
$65.00
$261.00
113
(3)

3-Methyladenine is an autophagy inhibitor that prevents the formation of autophagosomes. If DCAF16 is indirectly involved in autophagic degradation, inhibiting autophagosome formation could result in functional inhibition of DCAF16 due to disruption of this catabolic process.

Curcumin

458-37-7sc-200509
sc-200509A
sc-200509B
sc-200509C
sc-200509D
sc-200509F
sc-200509E
1 g
5 g
25 g
100 g
250 g
1 kg
2.5 kg
$37.00
$69.00
$109.00
$218.00
$239.00
$879.00
$1968.00
47
(1)

Curcumin has been known to interfere with the NF-κB pathway, which could indirectly affect DCAF16 if it is involved in the regulation of proteins under the control of NF-κB, leading to a decrease in ubiquitin-mediated protein degradation where DCAF16 might play a role.

PD 98059

167869-21-8sc-3532
sc-3532A
1 mg
5 mg
$40.00
$92.00
212
(2)

PD98059 is an inhibitor of MEK, which is part of the MAPK/ERK pathway. If DCAF16 is involved in signaling pathways downstream or upstream of MAPK/ERK, its activity could be indirectly inhibited by preventing the phosphorylation and subsequent activation of ERK, which may regulate proteins involved with DCAF16.

SB 203580

152121-47-6sc-3533
sc-3533A
1 mg
5 mg
$90.00
$349.00
284
(5)

SB203580 is a specific inhibitor of p38 MAPK, and if DCAF16 functions downstream of stress-activated pathways involving p38 MAPK, inhibiting this kinase could lead to a functional inhibition of DCAF16 through the disruption of these signaling pathways.

SP600125

129-56-6sc-200635
sc-200635A
10 mg
50 mg
$40.00
$150.00
257
(3)

SP600125 is an inhibitor of JNK, part of the MAPK family. Inhibition of JNK could indirectly impact DCAF16 function if DCAF16 is involved in pathways regulated by JNK, such as stress response or apoptosis-related protein degradation.