Date published: 2026-4-9

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FGFR-5 Activators

FGFR-5 Activators are a collection of compounds that enhance the functional activity of FGFR-5 through various signaling mechanisms. For instance, heparin and dibutyryl-cAMP elevate the receptors capacity to interact with its ligands and activate the associated kinase domain, respectively, further promoting autophosphorylation and downstream signaling cascades involved in cellular processes like proliferation and migration. Fibroblast Growth Factor Receptor-like 1 (FGFRL1) Activators encompass a variety of chemical compounds that indirectly potentiate the signaling pathways and biological processes associated with FGFRL1. Compounds such as Forskolin and Genistein facilitate this enhancement by increasing cAMP levels and inhibiting competitive tyrosine kinase activity, respectively, which can lead to the phosphorylation of FGFRL1 and a consequent enhancement of its cellular functions. Similarly, Sphingosine-1-phosphate and Thapsigargin act through lipid and calcium signaling to indirectly increase FGFRL1's role incell survival and angiogenesis. Phorbol 12-myristate 13-acetate (PMA) and Epigallocatechin gallate (EGCG) both contribute to this enhancement by modulating pathways that are shared with FGFRL1 functions, such as cell motility and morphogenesis for PMA, and through selective kinase inhibition that favors FGFRL1 signaling by EGCG. The activities of LY294002 and Wortmannin, both PI3K inhibitors, suggest a nuanced cellular environment where FGFRL1 pathways are upregulated due to the altered dynamics of the PI3K/Akt pathway, possibly enhancing the receptor's role in cell proliferation and survival. Moreover, the signaling equilibrium of FGFRL1 is further influenced by the presence of MAPK pathway modulators such as SB203580 and U0126, which by inhibiting p38 and MEK1/2, respectively, might create a cellular context that favors FGFRL1's involvement in differentiation and growth processes. Additionally, A23187 (Calcimycin) heightens FGFRL1 activity by increasing intracellular calcium, a crucial second messenger that intersects with FGFRL1 signaling to promote cellular adhesion and migration.
Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

Heparin

9005-49-6sc-507344
25 mg
$119.00
1
(0)

Heparin potentiates FGF-2 activity by facilitating its binding to FGFR-5, thereby enhancing the receptor's dimerization and activation, leading to increased downstream signaling and cellular responses.

SU 5402

215543-92-3sc-204308
sc-204308A
1 mg
5 mg
$63.00
$98.00
36
(3)

SU5402 is an FGFR inhibitor; however, at sub-inhibitory concentrations, it could potentially enhance FGFR-5 signaling by inducing a compensatory upregulation of the receptor's expression or sensitizing the receptor's kinase activity.

Dimethyl Sulfoxide (DMSO)

67-68-5sc-202581
sc-202581A
sc-202581B
100 ml
500 ml
4 L
$31.00
$117.00
$918.00
136
(6)

DMSO is known to affect membrane fluidity, which could hypothetically enhance FGFR-5 activation through improved receptor mobility and clustering, thus facilitating ligand-induced dimerization and activation.

Sodium Orthovanadate

13721-39-6sc-3540
sc-3540B
sc-3540A
5 g
10 g
50 g
$49.00
$57.00
$187.00
142
(4)

This compound is a phosphatase inhibitor that could enhance FGFR-5 signaling by preventing the dephosphorylation of the receptor's tyrosine residues, maintaining its active state and promoting prolonged signal transduction.

Forskolin

66575-29-9sc-3562
sc-3562A
sc-3562B
sc-3562C
sc-3562D
5 mg
50 mg
1 g
2 g
5 g
$78.00
$153.00
$740.00
$1413.00
$2091.00
73
(3)

Forskolin increases intracellular cAMP levels, which could enhance FGFR-5 activity by activating PKA, leading to phosphorylation events that promote FGFR-5 signaling pathways.

Lithium

7439-93-2sc-252954
50 g
$214.00
(0)

Lithium inhibits GSK-3, a negative regulator of many signaling pathways. Inhibition of GSK-3 could enhance FGFR-5 activity indirectly by modulating pathways that intersect with FGFR signaling.

β-Estradiol

50-28-2sc-204431
sc-204431A
500 mg
5 g
$63.00
$182.00
8
(1)

Estrogen can modulate the activity of various growth factor receptors. β-estradiol could potentially enhance FGFR-5 signaling by interacting with estrogen receptor pathways that crosstalk with tyrosine kinase receptor signaling.