Date published: 2025-10-25

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ADAMTS Activateurs

A Disintegrin and Metalloproteinase with Thrombospondin Motifs (ADAMTS) is a family of zinc-dependent extracellular enzymes that play a crucial role in a myriad of biological processes. These enzymes are active participants in the cleavage, restructuring, and maintenance of the extracellular matrix (ECM), which is a vital component of tissues and organs. Members of the ADAMTS family are involved in the proteolytic processing of various substrates within the ECM. Its signaling mechanisms are embedded within a web of regulatory pathways that include cytokine networks, growth factors, and other enzymes. These pathways modulate ADAMTS expression levels and enzymatic activity, implicating it in ECM remodeling, cell migration, and the modulation of other cellular behaviors. Factors like epigenetic regulation, substrate availability, and endogenous further add layers of complexity to the regulation of ADAMTS activity.

ADAMTS activators are aimed at understanding molecules that can specifically or indirectly modulate the activity of ADAMTS family members. While several types of molecules are being investigated for their role in activating or facilitating ADAMTS function, these range from small organic compounds to larger biological molecules. Small molecules like HDAC and TGF-β have been researched for their impact on the epigenetic and transcriptional regulation of ADAMTS family members, respectively. Others like MMP can indirectly contribute by preserving the availability of substrates in the ECM for ADAMTS proteins. Activators may also interact with ADAMTS members through various mechanisms such as inhibition of opposing pathways or through complex signaling cascades.

VOIR ÉGALEMENT...

Nom du produitCAS #Ref. CatalogueQuantitéPrix HTCITATIONS Classement

Suberoylanilide Hydroxamic Acid

149647-78-9sc-220139
sc-220139A
100 mg
500 mg
$130.00
$270.00
37
(2)

Les inhibiteurs d'HDAC peuvent influencer la régulation épigénétique de l'expression du gène ADAMTS-20.

SB 431542

301836-41-9sc-204265
sc-204265A
sc-204265B
1 mg
10 mg
25 mg
$80.00
$212.00
$408.00
48
(1)

En inhibant le TGF-β, ils pourraient potentiellement augmenter l'expression de l'ADAMTS-20 si le TGF-β est un suppresseur.

5-Azacytidine

320-67-2sc-221003
500 mg
$280.00
4
(1)

Les inhibiteurs de l'ADN-méthyltransférase pourraient affecter le statut de méthylation du gène ADAMTS-20, augmentant potentiellement son expression.

N-Acetyl-L-cysteine

616-91-1sc-202232
sc-202232A
sc-202232C
sc-202232B
5 g
25 g
1 kg
100 g
$33.00
$73.00
$265.00
$112.00
34
(1)

Peut activer l'ADAMTS-20 en réduisant les conditions de stress oxydatif qui l'inhibent autrement.

BAY 11-7082

19542-67-7sc-200615B
sc-200615
sc-200615A
5 mg
10 mg
50 mg
$61.00
$83.00
$349.00
155
(1)

Les inhibiteurs de NF-κB pourraient potentiellement réguler à la hausse l'ADAMTS-20 en supprimant la signalisation NF-κB, si le NF-κB agit comme un suppresseur.

XAV939

284028-89-3sc-296704
sc-296704A
sc-296704B
1 mg
5 mg
50 mg
$35.00
$115.00
$515.00
26
(1)

Les inhibiteurs de la voie Wnt peuvent influencer l'ADAMTS-20 en affectant la signalisation Wnt, dont on sait qu'elle est impliquée dans le remodelage de la MEC.

Gö 6983

133053-19-7sc-203432
sc-203432A
sc-203432B
1 mg
5 mg
10 mg
$103.00
$293.00
$465.00
15
(1)

Les inhibiteurs de la PKC pourraient influencer diverses voies de signalisation susceptibles d'activer indirectement l'ADAMTS-20.

Ruxolitinib

941678-49-5sc-364729
sc-364729A
sc-364729A-CW
5 mg
25 mg
25 mg
$246.00
$490.00
$536.00
16
(1)

Les inhibiteurs de JAK/STAT peuvent affecter la signalisation des cytokines qui influencent l'expression ou l'activité de l'ADAMTS-20.

Trametinib

871700-17-3sc-364639
sc-364639A
sc-364639B
5 mg
10 mg
1 g
$112.00
$163.00
$928.00
19
(1)

Les inhibiteurs de la MEK pourraient affecter les voies MAPK qui influencent l'ADAMTS-20.

Cobalt(II) chloride

7646-79-9sc-252623
sc-252623A
5 g
100 g
$63.00
$173.00
7
(1)

Les stabilisateurs HIF-1α pourraient potentiellement influencer l'activation ou l'expression d'ADAMTS-20 liée à l'hypoxie.