Supplementary Matrials

Supplementary Materials for:

A computationally identified compound antagonizes excess FGF-23 signaling in renal tubules and a mouse model of hypophosphatemia

Zhousheng Xiao, Demian Riccardi, Hector A. Velazquez, Ai L. Chin, Charles R. Yates, Jesse D. Carrick, Jeremy C. Smith, Jerome Baudry, L. Darryl Quarles*

*Corresponding author. Email: dquarles{at}uthsc.edu

This PDF file includes:

  • Fig. S1. RT-PCR analysis of FGFR isoforms and α-KL expression in HEK293T cells and human kidney total RNA.
  • Fig. S2. Quantification of phosphorylated FGFR1 abundance relative to that of total FGFR1 in cultured mouse primary tubule cells.
  • Fig. S3. Serum concentration of phosphate, PTH, and 1,25(OH)2D after 3 days of FGF-23 antagonist (Zinc13407541) injection in wild-type mice.
  • Table S1. Drug-like features of the four potential FGF-23 antagonists.
  • Table S2. Primer sequences.

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Citation: Z. Xiao, D. Riccardi, H. A. Velazquez, A. L. Chin, C. R. Yates, J. D. Carrick, J. C. Smith, J. Baudry, L. D. Quarles, A computationally identified compound antagonizes excess FGF-23 signaling in renal tubules and a mouse model of hypophosphatemia. Sci. Signal. 9, ra113 (2016).

© 2016 American Association for the Advancement of Science