Design, Synthesis, and Structure-Activity Relationship of Tetrahydropyrido[4,3-d]pyrimidine Derivatives as Potent Smoothened Antagonists with in Vivo Activity

ACS Chem Neurosci. 2017 Sep 20;8(9):1980-1994. doi: 10.1021/acschemneuro.7b00153. Epub 2017 Jun 30.

Abstract

Medulloblastoma is one of the most prevalent brain tumors in children. Aberrant hedgehog (Hh) pathway signaling is thought to be involved in the initiation and development of medulloblastoma. Vismodegib, the first FDA-approved cancer therapy based on inhibition of aberrant hedgehog signaling, targets smoothened (Smo), a G-protein coupled receptor (GPCR) central to the Hh pathway. Although vismodegib exhibits promising therapeutic efficacy in tumor treatment, concerns have been raised from its nonlinear pharmacokinetic (PK) profiles at high doses partly due to low aqueous solubility. Many patients experience adverse events such as muscle spasms and weight loss. In addition, drug resistance often arises among tumor cells during treatment with vismodegib. There is clearly an urgent need to explore novel Smo antagonists with improved potency and efficacy. Through a scaffold hopping strategy, we have identified a series of novel tetrahydropyrido[4,3-d]pyrimidine derivatives, which exhibited effective inhibition of Hh signaling. Among them, compound 24 is three times more potent than vismodegib in the NIH3T3-GRE-Luc reporter gene assay. Compound 24 has a lower melting point and much greater solubility compared with vismodegib, resulting in linear PK profiles when dosed orally at 10, 30, and 100 mg/kg in rats. Furthermore, compound 24 showed excellent PK profiles with a 72% oral bioavailability in beagle dogs. Compound 24 demonstrated overall favorable in vitro safety profiles with respect to CYP isoform and hERG inhibition. Finally, compound 24 led to significant regression of subcutaneous tumor generated by primary Ptch1-deficient medulloblastoma cells in SCID mouse. In conclusion, tetrahydropyrido[4,3-d]pyrimidine derivatives represent a novel set of Smo inhibitors that could potentially be utilized to treat medulloblastoma and other Hh pathway related malignancies.

Keywords: GPCR; Smoothened; antagonist; cancer therapy; hedgehog signaling pathway; medulloblastoma; scaffold hopping.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anilides / chemistry
  • Anilides / pharmacokinetics
  • Animals
  • Antineoplastic Agents / adverse effects
  • Antineoplastic Agents / chemical synthesis*
  • Antineoplastic Agents / pharmacokinetics
  • Antineoplastic Agents / pharmacology*
  • CHO Cells
  • Cerebellar Neoplasms / drug therapy
  • Cerebellar Neoplasms / metabolism
  • Cricetulus
  • Dogs
  • Drug Design
  • Female
  • Humans
  • Male
  • Medulloblastoma / drug therapy
  • Medulloblastoma / metabolism
  • Mice
  • Mice, Inbred ICR
  • Mice, SCID
  • Mice, Transgenic
  • NIH 3T3 Cells
  • Neoplasm Transplantation
  • Patched-1 Receptor / deficiency
  • Patched-1 Receptor / genetics
  • Pyridines / chemistry
  • Pyridines / pharmacokinetics
  • Pyrimidines / adverse effects
  • Pyrimidines / chemical synthesis*
  • Pyrimidines / pharmacokinetics
  • Pyrimidines / pharmacology*
  • Random Allocation
  • Rats, Sprague-Dawley
  • Smoothened Receptor / antagonists & inhibitors
  • Smoothened Receptor / metabolism
  • Structure-Activity Relationship
  • Transcriptional Regulator ERG / genetics
  • Transcriptional Regulator ERG / metabolism

Substances

  • Anilides
  • Antineoplastic Agents
  • ERG protein, human
  • HhAntag691
  • Patched-1 Receptor
  • Ptch1 protein, mouse
  • Pyridines
  • Pyrimidines
  • Smoothened Receptor
  • Transcriptional Regulator ERG