2. Immunology/Inflammation Metabolic Enzyme/Protease
  3. Nuclear Factor of activated T Cells (NFAT) Endogenous Metabolite
  4. GL64

GL64 is a selective agonist of ADGRD1 (EC50 = 3.98 μM). GL64 has low selectivity for ADGRD2, ADGRG5, ADGRG6, CELSR1, CELSR2, CELSR3, and ADGRG4 isoforms. GL64 activates ADGRD1 by mimicking the satchel sequence. GL64 regulates osteoclast maturation through the cAMP-PKA-NFATC1 pathway. GL64 effectively inhibits osteoclastogenesis and prevents bone loss both in vitro and in vivo. GL64 is useful in the study of osteoclast-related diseases.

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GL64

GL64 Chemical Structure

CAS No. : 488801-10-1

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GL64 Related Antibodies

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Description

GL64 is a selective agonist of ADGRD1 (EC50 = 3.98 μM). GL64 has low selectivity for ADGRD2, ADGRG5, ADGRG6, CELSR1, CELSR2, CELSR3, and ADGRG4 isoforms. GL64 activates ADGRD1 by mimicking the satchel sequence. GL64 regulates osteoclast maturation through the cAMP-PKA-NFATC1 pathway. GL64 effectively inhibits osteoclastogenesis and prevents bone loss both in vitro and in vivo. GL64 is useful in the study of osteoclast-related diseases[1].

In Vitro

GL64 (10 μM) stimulates CRE-luciferase activity by more than 1.5-fold in ADGRD1-overexpressing HEK293T cells[1].
GL64 (10 μM) increases CRE-luciferase and endogenous adenosine cAMP levels in wt MEFs but has no effect on Adgrd1−/− cells[1].
GL64 (0-100 μM) does not increase CRE-luciferase in HEK293T cells overexpressing adhesion GPCRs, such as ADGRD2, ADGRG5, ADGRG6, CELSR1, CELSR2, CELSR3, and ADGRG4, and does not activate nonadhesion GPCRs, including GPR68, NPFFR1, GPR183, and GPRC5B[1].
GL64 has weak agonist activity against ADGRD1 (EC50 = 16.89 μM) in stachel peptide-treated in ADGRD1-overexpressing HEK293T cells[1].
GL64 (10 μM, 6 days) inhibits the differentiation of male WT bone marrow-derived macrophages (BMMs) into mature osteoclasts but has no effect on Adgrd1−/− BMMs[1].
GL64 (10 μM, 6 days) down-regulates the mRNA expression levels of Dc-stamp, Acp5, and Nfatc1, during male mouse osteoclast maturation in BMMs[1].
GL64 (30 μM) increases endogenous cAMP levels in male BMMs[1].
GL64 (10 μM, 2 days) reduces NFATC1 nuclear localization in BMMs[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

GL64 Related Antibodies

RT-PCR[1]

Cell Line: BMMs
Concentration: 10 μM
Incubation Time: 6 days
Result: Down-regulateed the mRNA expression levels of Dc-stamp, Acp5, and Nfatc1.
In Vivo

GL64 (30 mg/kg, i.p., once a day, 4 weeks) rescues osteoclast hyperactivity and bone loss in Ovariectomy (OVX)-induced postmenopausal osteoporosis mice model[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: OVX-induced postmenopausal osteoporosis mice (twelve-week-old female C57BL/6J) model[1]
Dosage: 30 mg/kg
Administration: i.p., once a day, 4 weeks
Result: Rescued OVX-induced bone loss, increased BMD, BV/TV, and TB. N.
Inhibited OVX-induced TRAP expression and enzyme hyperactivity in femurs, reduced the osteoclast number and surface erosion, suppressed TRAP enzyme activity in the calvarias.
Molecular Weight

509.81

Formula

C27H19Cl3N2O2
CAS No.
SMILES

O=C1C2=CC=CC=C2NC(N1C3=CC=C(C=C3)Cl)C4=CC(OCC5=C(C=C(C=C5)Cl)Cl)=CC=C4
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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GL64 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

GL64488801-10-1GL 64GL-64Nuclear Factor of activated T Cells (NFAT)Endogenous MetaboliteAgonistHEK293T cellsBMMsOVX mice modelpostmenopausal osteoporosisInhibitorinhibitorinhibit

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