A computational investigation of the potential source of kinetic hindrance for the late appearance of pharmaceutically relevant stable forms of ritonavir, rotigotine, ranitidine hydrochloride, and pharmaceutical compound A was performed along the crystallization coordinates of the relative rates of conformational interconversion, crystal nucleation, and growth. Conformational distribution, classical nucleation, and growth morphol. theories were utilized, resp., to compare the results with those of polymorphic systems, famotidine, nimodipine, paracetamol, indomethacin, tolfenamic acid, and mebendazole for which kinetic hindrance of the stable forms was not reported. The results did not support a potential mechanism of kinetic hindering of the stable polymorphic form due to nucleation and growth limited crystallization However, a low population of crystallog. conformations of the stable forms in solution allowed us to distinguish the behavior of the late-appearing stable systems from other polymorphic systems. To account for the low crystallog. conformer population as the potential source for kinetic hindrance, we suggest that self-association of the monomeric active pharmaceutical ingredients mols. precedes over nucleation in solution As an implication to crystal structure prediction studies, it is suggested to complement the anal. of the lattice energy landscape of conformational polymorphs by the prediction of crystallog. conformers distribution in the gas phase and in solvents of potential interest. Computational investigation of a potential source of kinetic hindering of pharmaceutical conformational stable forms was performed along crystallization coordinates of the relative rates of conformational interconversion, crystal nucleation, and growth. For the polymorphic systems under consideration, an enriched selection of kinetically hindered stable forms was possible based on low populations of corresponding crystallog. conformations in solution