Date published: 2025-11-7

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TAJ-β Inhibidores

TAJ-β inhibitors represent a specialized class of chemical compounds designed to specifically inhibit the function of the TAJ-β protein, a molecule known to play a role in various cellular regulatory pathways. TAJ-β inhibitors operate by binding to the active sites or key functional domains of the TAJ-β protein, thus preventing its normal activity within the cell. These inhibitors are often developed to fit the precise structural features of the TAJ-β protein, ensuring that they can effectively block its interactions or catalytic actions. The inhibitors may target different regions of the protein, such as its binding pockets or allosteric sites, depending on their mode of action and the specific mechanism by which they interfere with the protein's function. The chemical design of TAJ-β inhibitors is crucial for achieving a high degree of specificity, ensuring they interact with TAJ-β while minimizing interaction with other proteins.

TAJ-β inhibitors are synthesized using advanced organic synthesis techniques that allow the precise assembly of molecules with defined structural features. These compounds often feature a combination of hydrophobic and hydrophilic regions that are designed to complement the three-dimensional shape of the TAJ-β protein. Some inhibitors may include functional groups capable of forming strong covalent or non-covalent bonds with the protein's active sites, thereby enhancing their inhibitory potency. The solubility, stability, and reactivity of these inhibitors are carefully considered during their design, as these properties influence how effectively the inhibitor can interact with TAJ-β under different conditions. The diversity in the structural composition of TAJ-β inhibitors allows for the fine-tuning of their binding affinities, making them a valuable class of compounds for studying the biochemical functions and regulatory mechanisms associated with the TAJ-β protein.

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Nombre del productoNÚMERO DE CAS #Número de catálogoCantidadPrecioMENCIONESClasificación

SB 202190

152121-30-7sc-202334
sc-202334A
sc-202334B
1 mg
5 mg
25 mg
¥338.00
¥1410.00
¥5020.00
45
(1)

Inhibe la p38 MAPK, afectando potencialmente a las vías de respuesta inflamatoria en las que podría estar implicada la TAJ-β.

LY 294002

154447-36-6sc-201426
sc-201426A
5 mg
25 mg
¥1365.00
¥4423.00
148
(1)

inhibidor de la PI3K, podría alterar vías de señalización importantes para la supervivencia y la proliferación celular.

SP600125

129-56-6sc-200635
sc-200635A
10 mg
50 mg
¥301.00
¥1128.00
257
(3)

inhibidor de JNK, podría influir en las vías de respuesta al estrés y la apoptosis relacionadas con la actividad de TAJ-β.

U-0126

109511-58-2sc-222395
sc-222395A
1 mg
5 mg
¥711.00
¥2719.00
136
(2)

inhibidor de MEK, afectando potencialmente a la vía MAPK/ERK, lo que podría ser relevante para la función de TAJ-β.

Wortmannin

19545-26-7sc-3505
sc-3505A
sc-3505B
1 mg
5 mg
20 mg
¥745.00
¥2471.00
¥4705.00
97
(3)

Otro inhibidor de PI3K, podría afectar aún más a las vías de señalización en las que se cree que participa TAJ-β.

Rapamycin

53123-88-9sc-3504
sc-3504A
sc-3504B
1 mg
5 mg
25 mg
¥699.00
¥1749.00
¥3610.00
233
(4)

inhibidor de mTOR, podría modular el crecimiento celular y los procesos de autofagia asociados a TAJ-β.

Sorafenib

284461-73-0sc-220125
sc-220125A
sc-220125B
5 mg
50 mg
500 mg
¥632.00
¥2933.00
¥4693.00
129
(3)

inhibidor de la quinasa RAF, podría afectar a las vías de crecimiento y diferenciación celular en las que interviene TAJ-β.

Z-VAD-FMK

187389-52-2sc-3067
500 µg
¥835.00
256
(6)

Inhibidor pan-caspasa, potencialmente influyente en las vías de apoptosis que TAJ-β podría regular.

Bortezomib

179324-69-7sc-217785
sc-217785A
2.5 mg
25 mg
¥1489.00
¥12004.00
115
(2)

inhibidor del proteasoma, podría afectar a las vías de degradación de proteínas relevantes para la función de TAJ-β.

Thalidomide

50-35-1sc-201445
sc-201445A
100 mg
500 mg
¥1230.00
¥3949.00
8
(0)

Modula el NF-κB y otras moléculas de señalización, afectando potencialmente a la inflamación y al crecimiento celular.