MK-3207 HCl

Catalog No.S1542

MK-3207 HCl Chemical Structure

Molecular Weight(MW): 594.05

MK-3207 is a potent CGRP receptor antagonist with IC50 and Kiof 0.12 nM and 0.022 nM, highly selective versus human AM1, AM2, CTR, and AMY3. Phase 2.

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2 Customer Reviews

  • (F) MK-3207 treatment led to a significant decrease of cAMP level (mean±SD, ***P<0.001). (G) Embryos treated with MK-3207 showed no obvious T cell or HSPC defects.

    Development, 2016, 143(12):2103-2110. . MK-3207 HCl purchased from Selleck.

    (E) and (F) Nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) p65 and DNA binding assays. Synoviocytes were pretreated with L-703606 or MK-3207 for 2 hours, followed by 1 hour of stimulation with SP (100 nM) or CGRP (1 nM). *P < 0.05 versus control. #P < 0.05 versus synoviocytes stimulated with SP or CGRP alone.

    Arthritis Res Ther, 2015.. MK-3207 HCl purchased from Selleck.

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Biological Activity

Description MK-3207 is a potent CGRP receptor antagonist with IC50 and Kiof 0.12 nM and 0.022 nM, highly selective versus human AM1, AM2, CTR, and AMY3. Phase 2.
Features The most potent orally active CGRP receptor antagonist described to date.
CGRP [1]
0.12 nM
In vitro

MK 3207 exhibits significantly higher affinity for both native and recombinant human CGRP receptor, as well as rhesus monkey CGRP receptor with Ki of 24 pM, ~24 pM and 22 pM, respectively, as compared to CGRP receptors from other species, including canine and rodent (Ki values of ~10 nM). Although has affinity for AMY1 (CTR/RAMP1) receptor with a Ki value of 0.75 nM, MK 3207 displays marked selectivity for human CGRP receptor versus related human AM1 (CLR/RAMP2) receptor, AM2 (CLR/RAMP3) receptor, AMY3 (CTR/RAMP3) receptor, and CTR with Ki values of 16.5 μM, 0.156 μM, 0.128 μM and 1.9 μM, respectively. MK 3207 potently inhibits human α-CGRP-induced cAMP production in HEK293 cells stably expressing human CLR/RAMP1 with an IC50 of 0.12 nM, and maintains similar potency in the presence of 50% human serum with an IC50 of 0.17 nM, indicating that the activity of MK 3207 would not be dramatically affected by plasma protein binding in vivo. MK 3207 exhibits approximately 65-fold more potent in the human serum-shifted in vitro functional assay than telcagepant with an IC50 of 10.9 nM. [1]

In vivo Administration of MK 3207 produces a concentration-dependent inhibition of capsaicin-induced dermal vasodilation in rhesus monkeys, blocking the blood flow increase with an EC50 of 0.8 nM and an EC90 of 7 nM, respectively. MK 3207 displays approximately 100-fold more potent in the rhesus monkey CIDV assay versus telcagepant with an EC90 of 994 nM. [1]


Animal Research:[1]
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  • Animal Models: Adult rhesus monkeys (either sex) with capsaicin-induced dermal vasodilation
  • Formulation: Dissolved in DMSO
  • Dosages: ~123.1 μg/kg
  • Administration: Intravenous bolus followed by 25 minutes continuous intravenous infusion
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 119 mg/mL (200.31 mM)
Ethanol 119 mg/mL (200.31 mM)
Water 5 mg/mL (8.41 mM)
In vivo Add solvents individually and in order:
1% DMSO+30% polyethylene glycol+1% Tween 80
30 mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 594.05


CAS No. 957116-20-0
Storage powder
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT00712725 Completed Migraine Merck Sharp & Dohme Corp. July 2008 Phase 2
NCT00548353 Completed Migraine Disorders Merck Sharp & Dohme Corp. August 2007 Phase 1

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Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID