Date published: 2026-5-30

1-800-457-3801

SCBT Portrait Logo
Seach Input

FSHR Inhibitors

FSHR inhibitors, short for Follicle-Stimulating Hormone Receptor inhibitors, belong to a distinct chemical class that plays a pivotal role in modulating reproductive processes within the body. These inhibitors target the Follicle-Stimulating Hormone Receptor (FSHR), a transmembrane protein that is predominantly expressed in reproductive tissues such as the ovaries and testes. The FSHR is an integral component of the reproductive endocrine system, facilitating the binding and signaling of the Follicle-Stimulating Hormone (FSH), a glycoprotein essential for normal sexual development and reproduction. FSHR inhibitors exert their effects by selectively binding to the FSHR, thereby interfering with the receptor's activation and downstream signaling pathways. Chemically, FSHR inhibitors exhibit structural diversity, but they commonly possess elements that allow them to interact with the FSHR's extracellular domains. This interaction impedes the natural binding of FSH to the receptor, disrupting the initiation of intracellular signaling cascades that are crucial for processes like folliculogenesis and spermatogenesis. The precise mechanism of action may vary among different FSHR inhibitors, but they share the common goal of modulating the receptor's function. Researchers have focused on developing FSHR inhibitors as tools to better understand the intricacies of reproductive biology and endocrine signaling, thereby expanding our comprehension of the physiological processes underlying fertility and sexual development.

The exploration of FSHR inhibitors offers insights into the complex interplay between hormones, receptors, and downstream cellular responses. By uncovering the molecular interactions that underlie FSH-FSHR binding and signaling disruption, scientists aim to unlock new avenues for research and potentially develop innovative strategies for manipulating reproductive processes. The chemical class of FSHR inhibitors serves as a valuable resource for investigating the regulatory mechanisms governing reproductive physiology, shedding light on the molecular underpinnings of fertility and opening doors to a deeper understanding of reproductive biology.

SEE ALSO...

Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

PKC-412

120685-11-2sc-200691
sc-200691A
1 mg
5 mg
$52.00
$114.00
10
(1)

Midostaurin inhibits FLT3 kinase activity by binding to the ATP-binding pocket, preventing phosphorylation and downstream signaling. It is approved for FLT3-mutated acute myeloid leukemia (AML) and systemic mastocytosis.

Sorafenib

284461-73-0sc-220125
sc-220125A
sc-220125B
5 mg
50 mg
500 mg
$57.00
$100.00
$250.00
129
(3)

Sorafenib inhibits FLT3, along with other kinases, by blocking ATP binding and disrupting the downstream signaling pathways. It has been investigated in AML and other malignancies.

Quizartinib, Free Base

950769-58-1sc-396767
sc-396767A
1 mg
5 mg
$68.00
$150.00
(0)

Quizartinib is a selective FLT3 inhibitor that competes with ATP for binding to FLT3, leading to inhibition of phosphorylation and downstream pathways. It's under investigation for FLT3-mutated AML.

Crenolanib

670220-88-9sc-364470
sc-364470A
5 mg
10 mg
$612.00
$1020.00
(1)

Crenolanib inhibits FLT3 signaling by targeting both FLT3-ITD and FLT3-TKD mutations, preventing autophosphorylation and downstream signaling pathways. It's being studied for AML and other malignancies.

KW 2449

1000669-72-6sc-364518
sc-364518A
10 mg
50 mg
$180.00
$744.00
(0)

KW-2449 is a FLT3 and ABL dual inhibitor that suppresses FLT3 autophosphorylation and downstream signaling pathways. It also inhibits ABL kinase, potentially offering broader anti-leukemic effects.

TG101209

936091-14-4sc-364731
sc-364731A
5 mg
50 mg
$255.00
$1455.00
(0)

TG101209 inhibits FLT3 kinase by binding to its ATP-binding site, inhibiting autophosphorylation and downstream signaling pathways.

Lestaurtinib

111358-88-4sc-218657
sc-218657A
sc-218657B
1 mg
5 mg
10 mg
$275.00
$326.00
$612.00
3
(1)

Lestaurtinib inhibits FLT3 autophosphorylation and downstream signaling by binding to the ATP-binding site of the kinase domain.