ABBV-167 is a phosphate prodrug of the BCL-2 inhibitor venetoclax.
分子量
978.45
Formula
C46H53ClN7O11PS
CAS 号
1351456-78-4
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Salem AH, et al. Expanding the Repertoire for “Large Small Molecules”: Prodrug ABBV-167 Efficiently Converts to Venetoclax with Reduced Food Effect in Healthy Volunteers. Mol Cancer Ther. 2021 Jun;20(6):999-1008.
ABBV-744 is a first-in-class, orally active and selective inhibitor of the BDII domain of BET family proteins with IC50 values ranging from 4 to 18 nM for BRD2, BRD3, BRD4 and BRDT. ABBV-744 is primarily metabolized by CYP3A4 with drug-like properties enable the investigation of its antitumor efficacy and tolerability[1].
IC50 & Target[1]
BRD2 (BD2)
8 nM (IC50)
BRD3 (BD2)
13 nM (IC50)
BRDT (BD2)
18 nM (IC50)
BRD4 (BD2)
4 nM (IC50)
BRD4 (BD2)
3 nM (Kd)
体外研究 (In Vitro)
ABBV-744 (90 nM; 0~24 h; LNCaP cells) downregulates the expression of KLK2 and MYC genes[1]. ABBV-744 (90 nM; 0~72 h; LNCaP cells) induces cell cycle arrest in G1 followed by senescence[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Western Blot Analysis[1]
Cell Line:
LNCaP cells
Concentration:
90 nM
Incubation Time:
0~24 hours
Result:
Downregulated the expression of KLK2 and MYC genes.
Cell Cycle Analysis[1]
Cell Line:
LNCaP cells
Concentration:
90 nM
Incubation Time:
0~72 hours
Result:
Induced cell cycle arrest in G1 followed by senescence.
体内研究 (In Vivo)
ABBV-744 (4.7 mg/kg; oral gavage; 28 days) causes a delay in tumor growth and displays equivalent or better antitumor activity compared with ABBV-075[1]. ABBV-744 (30 mg/kg; 14 days) is able to produce significant antitumor activity. ABBV-744 (30 mg/kg) triggers a reduction in platelets of only 20 %[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Mice
Dosage:
4.7 mg/kg (Pharmacokinetic Analysis)
Administration:
Oral gavage; 28 days
Result:
Caused a delay in tumor growth and displayed equivalent or better antitumor activity compared with ABBV-075.
Animal Model:
Sprague-Dawley rats
Dosage:
30 mg/kg (Pharmacokinetic Analysis)
Administration:
14 days
Result:
Produced significant antitumor activity.
Clinical Trial
分子量
491.55
Formula
C28H30FN3O4
CAS 号
2138861-99-9
运输条件
Room temperature in continental US; may vary elsewhere.
Mivebresib (ABBV-075) is a potent and orally active bromodomain and extraterminal domain (BET) bromodomain inhibitor. Mivebresib binds to BRD4 with a Ki of 1.5 nM[1].
IC50 & Target
IC50: 1.5 nM (BRD4)[1]
体外研究 (In Vitro)
Mivebresib inhibit DHT-stimulated transcription of AR target genes without significant effect on AR protein expression. In addition to blocking the transcription activation downstream of AR, Mivebresib is also a potent inhibitor of MYC and the TMPRSS2-ETS fusion proteins[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
分子量
459.47
Formula
C22H19F2N3O4S
CAS 号
1445993-26-9
中文名称
米维布塞
运输条件
Room temperature in continental US; may vary elsewhere.
将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中,再用生理盐水定容至 10 mL,完全溶解,澄清透明
*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献
[1]. EJ Faivre et al. Abstract 4694: ABBV-075, a novel BET family inhibitor, disrupts critical transcription programs that drive prostate cancer growth to induce potent anti-tumor activity in vitro and in vivo