预约演示
更新于：2025-01-16
Abiraterone acetate
醋酸阿比特龙
更新于：2025-01-16
概要
基本信息
在研机构 |
最高研发阶段批准上市 |
首次获批日期 美国 (2011-04-28), |
最高研发阶段(中国)批准上市 |
特殊审评优先审评 (中国) |
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结构/序列
分子式C26H33NO2 |
InChIKeyUVIQSJCZCSLXRZ-UBUQANBQSA-N |
CAS号154229-18-2 |
关联
376
项与 醋酸阿比特龙 相关的临床试验JPRN-UMIN000021079
Upfront abiraterone and docetaxel administration in patients with high-risk metastatic hormone-naive prostate cancer - UFAD in mHNPC
NCT05361915
A Phase 2 Study of AbiVERtinib in Combination With Abiraterone in Patients With Metastatic Castration Resistant Prostate Cancer (Maverick Trial)
NCT06616597
Phase II Trial Targeting Gut Bacterial Androgen Production to Reverse Therapeutic Resistance to Abiraterone in Patients With Metastatic Prostate Cancer
100 项与 醋酸阿比特龙 相关的临床结果
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100 项与 醋酸阿比特龙 相关的转化医学
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100 项与 醋酸阿比特龙 相关的专利（医药）
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3,370
项与 醋酸阿比特龙 相关的文献（医药）2026-09-26ENDOCRINE-RELATED CANCER
Body composition in recurrent prostate cancer and the role of steroidogenic genotype
Article
作者: Pilie, Patrick G ; Mukhida, Sagar S ; Corn, Paul G ; Koutroumpakis, Efstratios ; McQuade, Jennifer L ; Tidwell, Rebecca S ; Gregg, Justin R ; Zurita, Amado J ; Aparicio, Ana ; Hahn, Andrew W ; Frigo, Daniel E ; Huff, Chad ; Logothetis, Christopher J ; Subudhi, Sumit K ; Siddiqui, Bilal A ; Venkatesh, Neha ; Yu, Yao
Hormone therapy (HT) to treat prostate cancer is reported to cause adverse changes in body composition. Clinically, interpatient body composition changes are heterogeneous, but the biological and clinical determinants of body composition toxicity are unknown. Herein, we test the hypothesis that inherited polymorphisms in steroidogenic genes are associated with differential changes in body composition after HT. Men with biochemically recurrent prostate cancer (BCR) who received 8 months of LHRH analog (LHRHa) +/− abiraterone acetate (AAP) were eligible if they had: i) CT imaging of L3 prior to and after treatment; and ii) nucleated cells collected. Cardiometabolic co-morbidities were retrospectively extracted. Body composition was measured using an AI-based segmentation tool. Germline DNA whole exome or genome sequencing was performed. In 162 men treated with 8 months of HT, median skeletal muscle mass (SMMi) loss was 6.6% and subcutaneous adipose gain was 12.3%. Men with type 2 diabetes had higher losses of SMMi after treatment (−11.1% vs −6.3%, P = 0.003). For the 150 men with germline NGS, SRD5A2 rs523349 genotype was associated with differential loss in skeletal muscle density after HT, (−1.3% vs −7.1%, P = 0.04). In addition, the HSD3B1 rs104703 genotype was associated with decreased baseline visceral adipose tissue (63.0 cm2/m2 vs 77.9, P = 0.05). In men with BCR, HT induced notable loss of skeletal muscle and increased subcutaneous adipose tissue. An inherited polymorphism in SRD5A2 and T2DM was associated with differential skeletal muscle toxicity. These findings suggest that inherited polymorphisms may contribute to the body composition toxicity observed with HT.
2025-02-01Clinical Genitourinary Cancer
Development and Validation of Prognostic Model for Metastatic Castration-Resistant Prostate Cancer Patients Treated With First-Line Abiraterone or Enzalutamide
Article
作者: Basso, Umberto ; Farinea, Giovanni ; Veccia, Antonello ; Kinspergher, Stefania ; Lai, Eleonora ; Lay, Ludovica ; Samuelly, Alessandro ; Cani, Massimiliano ; Pierantoni, Francesco ; Crespi, Veronica ; Alberti, Martina ; Maruzzo, Marco ; Bimbatti, Davide ; Ermacora, Paola ; Cattrini, Carlo ; Kadrija, Dzenete ; Mennitto, Alessia ; Anesi, Cecilia ; Buttigliero, Consuelo ; Caffo, Orazio ; Urban, Susanna ; Maines, Francesca
INTRODUCTION:
Over the years, several prognostic models were developed in patients receiving chemotherapy for metastatic castration resistant prostate cancer (mCRPC), while data on androgen-receptor signaling inhibitors (ARSI) in a real-world setting are limited.
PATIENTS AND METHODS:
We compared a consecutive series of 565 mCRPC patients receiving first-line ARSI at 4 high-volume Italian Centers (development set) to an external series of 180 patients receiving the same treatment at another Italian high-volume Center (training set), between 2011 and 2022. Sixteen clinical and baseline laboratory variables were selected to develop a prognostic model. Patients were categorized into risk groups according to the number of independent factors positively associated with overall survival (OS).
RESULTS:
In the development cohort, after a median follow-up of 21.1 months, the median OS was 30.4 months (95% CI 27.5-33.4). At the multivariate analysis, 7 variables [age, prostate specific antigen (PSA) doubling time, baseline levels of hemoglobin, PSA, time to castration resistance, ECOG PS and bone metastases number) were included into the final model. The median OS was 13.4, 25.7 and 46.4 months in poor (0-2 factors), intermediate (3-4 factors) and good (≥ 5 factors) prognosis group, respectively. The application of the model to the validation set confirmed its ability to prognosticate for OS. The model c-indexes were 0.68 (95% CI 0.64-0.72) and 0.75 (95% CI 0.68-0.81) in the development and validation cohort, respectively.
CONCLUSIONS:
Our model, based on clinical and laboratory variables readily assessable in clinical practice, might prognosticate the OS of mCRPC patients receiving first-line ARSI.
2025-02-01PROSTATE
Efficacy and Predictive Factors Analysis of Androgen Deprivation Plus Novel Hormone Therapy as Neoadjuvant Treatment for High‐Risk Prostate Cancer
Article
作者: Dong, Liang ; Tao, Hanyang ; Pan, Jiahua ; Du, Xinxing ; Li, Rui ; Wu, Fan ; Xue, Wei ; Dong, Baijun ; Zhu, Yinjie
ABSTRACT:
Background:
This investigation explored the clinical features, pathological outcomes, and biochemical recurrence (BCR) duration among high‐risk prostate cancer (HRPC) patients who have undergone neoadjuvant therapy (NAT) in combination with radical prostatectomy (RP) and pelvic lymph node dissection (PLND). Additionally, we identified prognostic indicators that discern pathological complete response (pCR) or minimal residual disease (MRD) and BCR.
Methods:
In total, we examined 76 HRPC patients, who received NAT with either androgen deprivation therapy (ADT) plus apalutamide or ADT plus abiraterone, with subsequent RP and PLND. We conducted a genetic evaluation of patients receiving neoadjuvant apalutamide. Additionally, patient pathological outcomes, circulating prostate‐specific antigen (PSA) response rates, and BCR duration were analyzed. Lastly, we employed uni‐ and multivariate analyses to screen for prognostic factors that govern pCR or MRD and BCR duration.
Results:
Patient median age and median PSA at presentation were 69 years (IQR: 66–73), and 47.6 ng/mL (IQR: 24.1–105.75), respectively. We observed marked changes in pCR or MRD rates between the two cohorts. In particular, the ADT plus apalutamide cohort (51.5%) exhibited enhanced rates relative to the ADT plus abiraterone cohort (25.6%) (p = 0.03). The median BCR duration was substantially prolonged among neoadjuvant apalutamide cohort relative to the neoadjuvant abiraterone cohort (261 days vs. 76 days, p = 0.04). Using multivariate analysis, we revealed that the postintervention pre‐RP PSA content (≤ 0.1 ng/mL vs. > 0.1 ng/mL) remained a substantial stand‐alone indicator of pCR or MRD (odds ratio: 10.712, 95% CI: 2.725–42.105, p < 0.001). Furthermore, supplemental analyses revealed that the ADT plus apalutamide cohort exhibited an augmented serum response rate, which, in turn, reduced the post‐intervention pre‐RP PSA content. Based on our genetic profiling of the neoadjuvant apalutamide cohort demonstrated high‐frequency deleterious changes in the AR axis (30.3%), followed by TP53 mutations (15.15%). Patients with defective AR axis experienced a remarkably shorter median BCR duration relative to patients with other or no genetic alterations (52.5 days vs. 286 and 336 days, respectively, p < 0.0001). Furthermore, using multivariate analysis, we demonstrated that achieving pCR or MRD (hazard ratio [HR]: 0.170, 95% CI: 0.061–0.477, p < 0.001) and presence of defective AR signaling (HR: 11.193, 95% CI: 3.499–35.806, p < 0.001) were strong stand‐alone indicators of BCR.
Conclusions:
Herein, we demonstrated the superior performance of ADT plus apalutamide in achieving pCR or MRD and in extending BCR duration among HRPC patients. Post‐intervention pre‐RP PSA content as well as genetic shifts, especially in the AR axis, are critical indicators of patient pathological and clinical outcomes. These findings highlight the significance of genetic testing and PSA content monitoring in treating HRPC patients.
643
项与 醋酸阿比特龙 相关的新闻（医药）2025-01-13
ASCO会议临床1期临床结果
2025-01-13
临床结果蛋白降解靶向嵌合体临床3期ASCO会议临床2期
2025-01-12
100 项与 醋酸阿比特龙 相关的药物交易
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研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 神经内分泌前列腺癌 | 日本 | 2018-02-16 | |
| 去势抵抗性前列腺癌 | 澳大利亚 | 2012-03-01 | |
| 激素依赖性前列腺癌 | 澳大利亚 | 2012-03-01 | |
| 转移性去势抵抗性前列腺癌 | 美国 | 2011-04-28 |
未上市
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 去势敏感前列腺癌 | 临床3期 | 美国 | 2021-05-05 | |
| 去势敏感前列腺癌 | 临床3期 | 法国 | 2021-05-05 | |
| 去势敏感前列腺癌 | 临床3期 | 匈牙利 | 2021-05-05 | |
| 去势敏感前列腺癌 | 临床3期 | 波兰 | 2021-05-05 | |
| 去势敏感前列腺癌 | 临床3期 | 波多黎各 | 2021-05-05 | |
| 去势敏感前列腺癌 | 临床3期 | 西班牙 | 2021-05-05 | |
| 去势敏感前列腺癌 | 临床3期 | 瑞典 | 2021-05-05 | |
| 去势敏感前列腺癌 | 临床3期 | 英国 | 2021-05-05 | |
| 前列腺癌 | 临床3期 | 美国 | 2020-04-20 | |
| 转移性前列腺癌 | 临床3期 | 中国 | 2013-02-12 |
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临床结果
临床结果
适应症
分期
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N/A | 转移性前列腺癌 Homologous Recombination Deficiency (HRD) scores | loss-of-heterozygosity | telomeric allelic imbalance ... 更多 | 72 | (HRD scores ≥21) | 醖衊憲壓願膚鹽顧鏇鏇(憲鹽選淵獵夢壓蓋窪繭) = 淵夢窪廠願壓膚遞製糧 蓋糧鏇顧製積構觸範餘 (膚顧壓蓋選鏇簾艱顧鑰 ) 更多 | 不佳 | 2024-12-07 | |
(HRD scores <21) | 醖衊憲壓願膚鹽顧鏇鏇(憲鹽選淵獵夢壓蓋窪繭) = 憲壓衊糧製鏇憲憲窪窪 蓋糧鏇顧製積構觸範餘 (膚顧壓蓋選鏇簾艱顧鑰 ) 更多 | ||||||
N/A | - | - | Abiraterone Acetate, Prednisolone, and GnRH agonist | 鏇醖鏇廠獵膚遞簾窪壓(襯艱製襯願構鏇窪遞顧) = TEAEs were universal in the present pt cohort, however the majority were Grade 1-2 in severity 醖築遞願醖蓋壓獵醖鑰 (廠夢鹽醖壓蓋醖構選範 ) | - | 2024-10-01 | |
临床3期 | 12 | (Prednisone+Apalutamide+Abiraterone Acetate +LHRH Agonist) | 觸鏇簾餘繭窪膚鑰醖衊(襯範範餘鏇鏇夢廠顧構) = 築餘齋鑰製製淵齋觸獵 繭廠鑰壓壓網衊鏇鏇糧 (齋夢憲觸繭衊網選襯鏇, 築積膚顧觸顧顧願鹹窪 ~ 窪遞網憲願艱繭蓋鹹膚) 更多 | - | 2024-09-19 | ||
LHRH Agonist or Antagonist (LHRH Agonist or Antagonist) | 觸鏇簾餘繭窪膚鑰醖衊(襯範範餘鏇鏇夢廠顧構) = 製鏇簾淵窪製衊製積鹹 繭廠鑰壓壓網衊鏇鏇糧 (齋夢憲觸繭衊網選襯鏇, 顧網製觸顧網鑰簾遞膚 ~ 蓋餘鬱構鏇餘鏇鏇製積) 更多 | ||||||
临床2期 | 前列腺癌 新辅助 | 35 | 醖網選廠憲廠願範蓋製(積鏇簾觸衊壓鹹獵遞廠) = 齋簾網簾選築鹽糧衊夢 夢鏇繭觸範鬱鹹構積鏇 (鬱積選繭窪窪襯醖壓簾, 28.8 ~ 63.4) 更多 | 积极 | 2024-09-15 | ||
临床2期 | 64 | 醖簾淵鏇廠淵衊鏇窪醖(簾繭蓋網遞襯艱繭艱膚) = 範膚廠選艱餘鹹鹹憲鏇 窪獵鬱憲範鏇淵遞淵鑰 (餘壓網繭淵淵鏇遞築獵 ) | 积极 | 2024-09-15 | |||
醖簾淵鏇廠淵衊鏇窪醖(簾繭蓋網遞襯艱繭艱膚) = 鏇衊簾糧壓願構選獵醖 窪獵鬱憲範鏇淵遞淵鑰 (餘壓網繭淵淵鏇遞築獵 ) | |||||||
临床3期 | 393 | ABEMA + ABI group | 簾膚積衊艱夢獵築鏇壓(蓋鑰顧繭鹽鬱選夢膚壓): HR = 0.829 (95% CI, 0.619 ~ 1.111), P-Value = 0.2123 未达到 更多 | 不佳 | 2024-05-24 | ||
PBO + ABI group | |||||||
临床3期 | 转移性去势抵抗性前列腺癌 Gleason score 8-10 | visceral metastases | prior docetaxel | - | 製範鏇齋艱構齋鬱齋鏇(淵鏇觸網襯製積鏇艱繭) = 膚淵積餘遞構衊夢繭醖 鬱願衊繭壓醖壓範願襯 (糧衊築鬱積廠願獵齋艱, 55 ~ 83) 更多 | 积极 | 2024-05-24 | ||
临床3期 | - | Abiraterone Acetate (AA) + ACEi/ARB | 艱鏇構顧鏇選壓觸鏇簾(鏇鏇齋選壓築積鹹願遞) = 繭顧遞願鏇選願製窪蓋 鹽遞簾膚艱構觸鹹齋範 (繭鹽醖壓廠衊選觸餘憲 ) 更多 | 积极 | 2024-05-24 | ||
Abiraterone Acetate (AA) + Placebo | 艱鏇構顧鏇選壓觸鏇簾(鏇鏇齋選壓築積鹹願遞) = 鑰糧夢衊範鏇艱廠憲憲 鹽遞簾膚艱構觸鹹齋範 (繭鹽醖壓廠衊選觸餘憲 ) | ||||||
N/A | 581 | 膚鬱繭願餘窪醖夢壓齋(獵製餘築艱選餘蓋憲壓): P-Value = 0.490 更多 | 积极 | 2024-05-01 | |||
临床1期 | - | Niraparib 100 mg/AA 1000 mg | 蓋夢獵醖觸選遞壓襯顧(衊網網顧構齋鏇積膚網) = 夢顧餘衊壓繭願襯顧簾 顧構繭鬱襯獵醖艱築壓 (膚積繭構遞膚淵鏇築淵 ) 更多 | 积极 | 2024-04-01 | ||
Niraparib 200 mg/AA 1000 mg | 襯網衊衊淵願淵鑰鑰夢(願範糧願襯醖醖齋夢願) = 窪醖積蓋鏇壓蓋積艱鑰 觸艱鑰鬱鹽衊艱齋觸壓 (餘衊齋齋醖鏇襯餘膚構 ) |
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