Crystallization of Amorphous Pharmaceuticals at Ambient and Elevated …
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a
b
c
d
e
f
g
h
Fig. 2 Dielectric spectra of four selected APIs: a and b FLU, c and d NIM, e and f EZB and g and
h PBC, measured at ambient pressure and at different temperatures above their T g
final metabolic pathway. It also acts as an inhibitor of the initial stages of cholesterol
synthesis, blocks the oxidation and tissue deposition of LDL cholesterol, thereby
inhibiting atherogenesis.
As can be seen in Fig. 2 a, c, e, and f, on the dielectric loss spectra of amorphous
pharmaceuticals, which were register at T > T g , one might notice even three features.
Beginning from the lowest frequencies: (i) the dc conductivity associated with translational motions of ions (see loss spectra of NIM and EZB); (ii) the well-resolved
loss peak associated with the structural (α; global) relaxation process (visible in all
presented cases); as well as (iii) the secondary (β; local) relaxation peak of much
weaker than α-relaxation amplitude (see loss spectra of PBC and NIM).
61
a
b
c
d
e
f
g
h
Fig. 2 Dielectric spectra of four selected APIs: a and b FLU, c and d NIM, e and f EZB and g and
h PBC, measured at ambient pressure and at different temperatures above their T g
final metabolic pathway. It also acts as an inhibitor of the initial stages of cholesterol
synthesis, blocks the oxidation and tissue deposition of LDL cholesterol, thereby
inhibiting atherogenesis.
As can be seen in Fig. 2 a, c, e, and f, on the dielectric loss spectra of amorphous
pharmaceuticals, which were register at T > T g , one might notice even three features.
Beginning from the lowest frequencies: (i) the dc conductivity associated with translational motions of ions (see loss spectra of NIM and EZB); (ii) the well-resolved
loss peak associated with the structural (α; global) relaxation process (visible in all
presented cases); as well as (iii) the secondary (β; local) relaxation peak of much
weaker than α-relaxation amplitude (see loss spectra of PBC and NIM).