Date published: 2026-4-24

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TREX-1 Activators

The chemical class of TREX-1 activators constitutes a multifaceted array of compounds, each with unique mechanisms shaping TREX-1 activation through nuanced modulation of diverse cellular pathways. An exemplar within this class, Nordihydroguaiaretic acid (NDGA), operates by indirect activation of TREX-1 through inhibition of the NF-κB pathway. Given that NF-κB acts as a negative regulator of TREX-1, NDGA's intervention effectively alleviates this inhibition, resulting in augmented TREX-1 activation. In a distinct modulatory approach, Resveratrol emerges as another activator, influencing TREX-1 indirectly by orchestrating the SIRT1 pathway. Serving as a SIRT1 activator, Resveratrol enhances the deacetylation of p53, a positive regulator of TREX-1 expression. This intricate interplay presents a unique mechanism for TREX-1 activation, expanding the repertoire of pathways involved.

The chemical class further encompasses a spectrum of compounds such as 6-Mercaptopurine, Ciclopirox olamine, Quinacrine, Piperlongumine, Mefloquine, Digoxin, Berberine, Metformin, Bortezomib, and Chloroquine. Each of these compounds exerts its influence on specific pathways, indirectly activating TREX-1. This diversity not only furnishes researchers with a comprehensive toolkit for precise modulation of TREX-1 but also underscores the complex and interconnected nature of cellular pathways involved in TREX-1 activation. 6-Mercaptopurine, for instance, impacts nucleotide metabolism, influencing TREX-1 activation. Ciclopirox olamine, a known antifungal, demonstrates its indirect impact on TREX-1 through distinct cellular pathways. Similarly, the array of compounds within this class showcases a rich tapestry of interactions, collectively contributing to the nuanced regulation of TREX-1. In summary, the intricate modulation of TREX-1 by this chemical class reflects a sophisticated dance of molecular interactions, unveiling the interconnectedness of various cellular pathways in shaping TREX-1 activation. This expansive toolkit not only enhances our understanding of TREX-1 regulation but also provides valuable insights for researchers exploring the broader landscape of cellular processes influenced by these chemical modulators.

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Items 1 to 10 of 11 total

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Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

NDGA (Nordihydroguaiaretic acid)

500-38-9sc-200487
sc-200487A
sc-200487B
1 g
5 g
25 g
$109.00
$384.00
$2190.00
3
(1)

NDGA is a potent inhibitor of the NF-κB pathway, exerting its influence through the inhibition of IKK activity. By impeding NF-κB signaling, NDGA indirectly activates TREX-1, as NF-κB negatively regulates TREX-1 expression, and its inhibition relieves this constraint.

Resveratrol

501-36-0sc-200808
sc-200808A
sc-200808B
100 mg
500 mg
5 g
$80.00
$220.00
$460.00
64
(2)

Resveratrol, a polyphenolic compound, indirectly activates TREX-1 by modulating the SIRT1 pathway. Acting as a SIRT1 activator, resveratrol enhances SIRT1-mediated deacetylation of p53. Deacetylated p53 positively regulates TREX-1 expression, providing an indirect mechanism for the activation of TREX-1.

6-Mercaptopurine

50-44-2sc-361087
sc-361087A
50 mg
100 mg
$72.00
$104.00
(0)

As an immunosuppressive agent, 6-Mercaptopurine indirectly activates TREX-1 by influencing the purine metabolism pathway. By inhibiting key enzymes in purine synthesis, it leads to the accumulation of endogenous nucleotides, triggering the cGAS-STING pathway. The resultant cGAS-STING activation positively regulates TREX-1 expression.

Ciclopirox

29342-05-0sc-217893
25 mg
$207.00
2
(1)

Ciclopirox olamine indirectly activates TREX-1 by targeting the AMPK pathway. Through AMPK activation, Ciclopirox olamine modulates cellular energy status, leading to downstream effects on p53. Activated p53 positively regulates TREX-1 expression, establishing an indirect link between Ciclopirox olamine and TREX-1 activation.

Quinacrine, Dihydrochloride

69-05-6sc-204222
sc-204222B
sc-204222A
sc-204222C
sc-204222D
100 mg
1 g
5 g
200 g
300 g
$46.00
$57.00
$87.00
$3257.00
$4821.00
4
(2)

Quinacrine indirectly activates TREX-1 through the modulation of autophagy. By inhibiting lysosomal function, Quinacrine disrupts the autophagic flux, leading to the accumulation of damaged DNA. This activates the cGAS-STING pathway, which positively regulates TREX-1 expression, establishing an indirect mechanism for TREX-1 activation.

Piperlongumine

20069-09-4sc-364128
10 mg
$107.00
(1)

Piperlongumine indirectly activates TREX-1 by targeting the NRF2 pathway. Through NRF2 activation, Piperlongumine upregulates the expression of antioxidants, leading to the attenuation of oxidative stress. Reduced oxidative stress positively regulates TREX-1 expression, establishing an indirect link between Piperlongumine and TREX-1 activation.

12β-Hydroxydigitoxin

20830-75-5sc-213604
sc-213604A
1 g
5 g
$143.00
$694.00
(0)

12β-Hydroxydigitoxin (Digoxin) indirectly activates TREX-1 by influencing the calcium signaling pathway. By inhibiting the Na+/K+-ATPase pump, Digoxin increases intracellular calcium levels, leading to the activation of the cGAS-STING pathway. Activated cGAS-STING positively regulates TREX-1 expression, establishing an indirect link between Digoxin and TREX-1 activation.

Berberine

2086-83-1sc-507337
250 mg
$92.00
1
(0)

Berberine indirectly activates TREX-1 by targeting the SIRT1 pathway. As a SIRT1 activator, Berberine enhances the deacetylation of p53. Deacetylated p53 positively regulates TREX-1 expression, providing an indirect mechanism for the activation of TREX-1.

Metformin

657-24-9sc-507370
10 mg
$79.00
2
(0)

Metformin indirectly activates TREX-1 through the modulation of the AMPK pathway. AMPK activation by Metformin influences cellular energy homeostasis, leading to downstream effects on p53. Activated p53 positively regulates TREX-1 expression, establishing an indirect link between Metformin and TREX-1 activation.

Bortezomib

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

Bortezomib indirectly activates TREX-1 by targeting the NF-κB pathway. Through the inhibition of the proteasome, Bortezomib disrupts NF-κB signaling, relieving its negative regulation on TREX-1 expression. This establishes an indirect mechanism for TREX-1 activation by Bortezomib.