1330286-47-9

Basic information

• Product Name: BOC-TRANS-4-FLUORO-L-PROLINONITRILE
• Synonyms: BOC-TRANS-4-FLUORO-L-PROLINONITRILE;N-T-BOC-TRANS-4-FLUORO-L-PROLINONITRILE;(2S,4R)-tert-Butyl 2-cyano-4-fluoropyrrolidine-1-carboxylate
• CAS NO: 1330286-47-9
• Molecular Formula: C₁₀H₁₅FN₂O₂
• Molecular Weight: 214.24
• Mol File: 1330286-47-9.mol

Chemical Properties

• Appearance: /
• CAS DataBase Reference: BOC-TRANS-4-FLUORO-L-PROLINONITRILE(CAS DataBase Reference)
• NIST Chemistry Reference: BOC-TRANS-4-FLUORO-L-PROLINONITRILE(1330286-47-9)
• EPA Substance Registry System: BOC-TRANS-4-FLUORO-L-PROLINONITRILE(1330286-47-9)

Safety Data

• Statements: 43
• Safety Statements: 36/37
• Hazardous Substances Data: 1330286-47-9(Hazardous Substances Data)

Upstream product

• 426844-26-0 tert-butyl (2S,4R)-2-carbamoyl-4-fluoropyrrolidine-1-carboxylate 

Downstream Products

• 1584652-41-4 (2S,4R)-4-fluoropyrrolidine-2-carbonitrile 4-methylbenzenesulfonic acid 

Relevant articles and documents

Extended structure-activity relationship and pharmacokinetic investigation of (4-quinolinoyl)glycyl-2-cyanopyrrolidine inhibitors of fibroblast activation protein (FAP)

Fibroblast activation protein (FAP) is a serine protease related to dipeptidyl peptidase IV (DPPIV). It has been convincingly linked to multiple disease states involving remodeling of the extracellular matrix. FAP inhibition is investigated as a therapeutic option for several of these diseases, with most attention so far devoted to oncology applications. We previously discovered the N-4-quinolinoyl-Gly-(2S)-cyanoPro scaffold as a possible entry to highly potent and selective FAP inhibitors. In the present study, we explore in detail the structure-activity relationship around this core scaffold. We report extensively optimized compounds that display low nanomolar inhibitory potency and high selectivity against the related dipeptidyl peptidases (DPPs) DPPIV, DPP9, DPPII, and prolyl oligopeptidase (PREP) the log D values, plasma stabilities, and microsomal stabilities of selected compounds were found to be highly satisfactory. Pharmacokinetic evaluation in mice of selected inhibitors demonstrated high oral bioavailability, plasma half-life, and the potential to selectively and completely inhibit FAP in vivo.