Estradiol-17β [BSA] (DAG2984)

Estradiol-17β, BSA-Conjugated, synthetic

Product Overview
Estradiol, BSA-Conjugated
1.0 mg/mL
1 mg
Supplied in 15 mM KPO4, 0.85% NaCl, pH 7.2
0.1% Sodium Azide
2-8°C short term, -20°C long term
PLEASE note that this product is intended for research use only; not for diagnostic or clinical use.
17 beta Estradiol is a steriod hormone that is produced in the ovary, placenta, testis, and possibly the adrenal cortex.
17 beta Oestradiol; estradiol


Have you cited DAG2984 in a publication? Let us know and earn a reward for your research.

Related Products

Estradiol [AP] (DAG2986)
Estradiol [BSA] (DAGA-025B)
Estradiol [KLH] (DAGA-028K)
Estradiol [HRP] (DAGA-025B-HRP)

Customer Reviews

Write a review, share your experiences with others and get rewarded !
Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket
Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket


Pediatric pituitary adenoma with mixed FSH and TSH immunostaining and FSH hypersecretion in a 6 year-old girl with precocious puberty: case report and multidisciplinary management


Authors: Ceraudo, Marco; Criminelli Rossi, Diego; Di Iorgi, Natascia; Cama, Armando; Piatelli, Gianluca; Consales, Alessandro

Objective We describe a rare case of functioning gonadotropins-producing pediatric adenoma immunostaining positively for FSH and focally for TSH causing central precocious puberty associated to central hypothyroidism in a 6 year-old girl. Materials and Methods Clinical evaluation revealed precocious puberty, as confirmed by hormonal determination with elevated FSH and estradiol, while central hypothyroidism was biochemically diagnosed by a low fT4 and normal TSH. Head MRI showed the presence of a hyperintense pituitary lesion. The patient successfully underwent transsphenoidal endoscopic resection of the pituitary macroadenoma. Results Pathologic evaluation of the tissue resected at surgery confirmed the diagnosis of pituitary adenoma with positive immunohistochemistry for FSH and focally for TSH in a mixed pattern. Ten months after surgery, there were no neurological signs and symptoms. Postoperative head MRI showed no abnormalities and no evidence of tumor regrowth. Conclusions Early and accurate diagnosis, multidisciplinary approach and close follow up are crucial factors for the favorable outcome.

Fatty Acid Synthase Is a Key Enabler for Endocrine Resistance in Heregulin-Overexpressing Luminal B-Like Breast Cancer


Authors: Menendez, Javier A.; Mehmi, Inderjit; Papadimitropoulou, Adriana; Vander Steen, Travis; Cuyas, Elisabet; Verdura, Sara; Espinoza, Ingrid; Vellon, Luciano; Atlas, Ella; Lupu, Ruth

HER2 transactivation by the HER3 ligand heregulin (HRG) promotes an endocrine-resistant phenotype in the estrogen receptor-positive (ER+) luminal-B subtype of breast cancer. The underlying biological mechanisms that link them are, however, incompletely understood. Here, we evaluated the putative role of the lipogenic enzyme fatty acid synthase (FASN) as a major cause of HRG-driven endocrine resistance in ER+/HER2-negative breast cancer cells. MCF-7 cells engineered to stably overexpress HRG (MCF-7/HRG), an in vitro model of tamoxifen/fulvestrant-resistant luminal B-like breast cancer, showed a pronounced up-regulation of FASN gene/FASN protein expression. Autocrine HRG up-regulated FASN expression via HER2 transactivation and downstream activation of PI-3K/AKT and MAPK-ERK1/2 signaling pathways. The HRG-driven FASN-overexpressing phenotype was fully prevented in MCF-7 cells expressing a structural deletion mutant of HRG that is sequestered in a cellular compartment and lacks the ability to promote endocrine-resistance in an autocrine manner. Pharmacological inhibition of FASN activity blocked the estradiol-independent and tamoxifen/fulvestrant-refractory ability of MCF-7/HRG cells to anchorage-independently grow in soft-agar. In vivo treatment with a FASN inhibitor restored the anti-tumor activity of tamoxifen and fulvestrant against fast-growing, hormone-resistant MCF-7/HRG xenograft tumors in mice. Overall, these findings implicate FASN as a key enabler for endocrine resistance in HRG+/HER2- breast cancer and highlight the therapeutic potential of FASN inhibitors for the treatment of endocrine therapy-resistant luminal-B breast cancer.

Online Inquiry

Phone: *
E-mail Address: *
Technology Interest:
Type of Organization:
Service & Products Interested: *
Project Description:

Related Products

Related Resources

Ordering Information

Payment methods we support:
Invoice / Purchase Order
Credit card

Inquiry Basket