What happens at the surface of a PVPVA dispersion during dissolution that makes release collapse above the LoC, and why does phenolphthalein reach that point at a much lower drug loading than its methoxy derivative?
Water splits the gel layer into a drug-rich and a water-rich phase; while the drug-rich phase stays as droplets below 1 μm release is good, and once it connects into a network a porous drug-rich layer stays on the surface and release stops. ····· Networks appeared at 40-50% DL for MePHPH but already at 10-20% DL for PHPH, whose drug-rich phase was about three-quarters polymer (26.2 wt% drug, dry basis) against 98.8 wt% drug for MePHPH. ··
For MePHPH and PHPH in PVPVA compacts at 37 °C in pH 6.8 buffer, the authors conclude that in both systems the loss of congruency came from a continuous hydrophobic network formed in the gel layer by water-induced phase separation, which acted as a barrier to release; the abstract words this as a correlation ("was found to correlate"), the conclusions as a cause ("was due to"). · Below the LoC the drug-rich phase forms discrete nanoparticles that leave with the dissolving polymer, inside the gel for MePHPH and, at 5% DL PHPH, apparently outside it ("appear to originate outside the gel layer"). ·· The lower LoC of PHPH is attributed to the polymer carried into its hydrophobic phase, which enlarges that phase; hydrogen bonding as the cause is taken from earlier work and was not measured here. ·· Because drug accumulated in the gel at 40% DL, the authors suggest the true MePHPH LoC lies below the cited 40% ("This suggests"). · They propose that the congruent release rate is set by water penetration and polymer chain disentanglement ("it was proposed"), and that the plait point of the drug-polymer-water phase diagram "serves as an arbiter for approximating the maximum LoC". · Two key links were not measured: no phase diagram was measured or computed for these systems, and the barrier role rests on images and release taken in separate experiments, without a measurement of transport through the network. ·
01Why this study
Below the LoC drug and polymer leave together and completely; above it drug release falls off a cliff, most clearly for copovidone ASDs.
Water-induced AAPS, thermodynamically the same as LLPS, has been proposed at the dissolving surface but is rarely watched in situ.
Purohit 2017, ref 11; Han 2019, ref 19
A continuous hydrophobic phase was proposed to give incongruent release, discrete domains congruent release.
Han 2019, ref 19
In PVPVA their LoCs are 5% and 40% DL, and strong drug-polymer interaction lowers the LoC.
Que 2021, ref 23 ·
More detail
What was already known. The introduction builds on these points, most of them from the Taylor group:
- Polymers also drive release. The polymer in an ASD was long seen as a crystallization inhibitor, but its role in enhancing drug release is now stressed. (Qian 2010, ref 4; Indulkar 2019, ref 8)
- Congruent release. In copovidone ASDs at low DL the drug and polymer percent release rates are similar and release runs to completion; apparent drug concentrations can exceed the amorphous solubility, and drug-rich nanoparticles form by LLPS. (Ilevbare 2013, ref 9; Que 2019, ref 10; Purohit 2017, ref 11) An isotope-scrambling study placed nanoparticle formation in a high-mobility environment, in solution or in a low-viscosity region near the interface. (Indulkar 2017, ref 12)
- Falling off a cliff. At high DL the two rates diverge and both decline, the drug more strikingly; at still higher DL both stop, possibly a third regime. The LoC is the DL where congruent release ends; reported values range from 5 to 40% DL. (refs 8, 10, 13-16, 23) ·
- AAPS at the interface. Water-induced AAPS is the same thermodynamic phenomenon as LLPS in a different concentration range; it has been studied for processing and storage and proposed at the dissolving surface, but not typically studied in situ. (Saboo 2017, ref 17; Rumondor 2009, ref 18; Purohit 2017, ref 11; Han 2019, ref 19)
- A surface barrier. AAPS has been postulated to create an amorphous insoluble barrier on the surface, reported drug-rich or polymer-containing, with polymer up to about 75% for a phenolic compound in copovidone. (Indulkar 2019, ref 8; Saboo 2020, ref 13; Deac 2023a, ref 22) ·
- Morphology hypothesis. Han and coworkers proposed that a hydrophobic phase forming a continuous network gives incongruent release, and discrete hydrophobic domains in a continuous hydrophilic phase give congruent release, the domains dispersing into the bulk. (Han 2019, ref 19)
- What moves the LoC. Adhesive drug-polymer interaction strength (Saboo 2020, ref 13; Que 2021, ref 23), drug Tg (ref 13; Hiew 2022, ref 24) and additives (refs 10, 25-27) have been suggested.
- The model compounds. Phenolphthalein and its methoxy derivative have low (5%) and high (40%) LoCs as copovidone ASDs. (Que 2021, ref 23)
What the paper set out to do. Develop an in situ confocal method to see phase separation at the ASD/solution interface during hydration and release; use it, with release tests and gel-layer analysis (composition, thickness, residence time), to explain the release profiles and probe what sets the LoC; measure the Tg and composition of the hydrophobic phase formed during release; and build a framework for qualitative LoC prediction for binary ASDs.
02How they approached it
Two analogues on one scaffold: PHPH has two phenolic OH groups that can hydrogen-bond to PVPVA, MePHPH has them methylated. Loadings span each cited LoC, and every experiment uses pH 6.8, 50 mM phosphate buffer at 37 °C. ·····
What was done
Compacts with a 0.5 cm² face in 100 mL buffer at 100 rpm→drug and polymer release at 10, 20, 30 min→gel scraped off, weighed, analysed→thickness, water, drug content, residence time.·······
Dye-labelled compacts (prodan blue, rhodamine 6G red) in buffer→confocal imaging of the dissolving edge every 30 s→onset position and morphology of the separated phases.····
Compacts dissolved 2-20 min, then removed→confocal imaging of the surface and of cross-sections.····
Compacts fully released at 500 rpm→nanoparticles centrifuged→drug content (HPLC) and Tg (DSC).··
Morphology at each DL set against release and gel data→network formation linked to loss of congruency.··
Polymer dissolution theory and schematic type I phase diagrams→qualitative framework in which the plait point sets the maximum LoC.···
More detail
What was done
- ASDs and compacts. Drug and PVPVA were dissolved in ethanol and rotary-evaporated; ASDs for imaging also contained 0.05 w/w% rhodamine 6G and 0.1 w/w% prodan. 100-200 mg of ASD was pressed at 1500 psi for 60 s in a Wood intrinsic die exposing 0.5 cm². ···
- Release and gel layer. Compacts dissolved in 100 mL pH 6.8, 50 mM phosphate buffer at 37 °C and 100 rpm; drug and polymer were measured by HPLC at 10, 20 and 30 min (percent release on a 100 mg basis, n = 3 per time point). At each time point the run was stopped, the gel was scraped off within 2 min, weighed, dissolved in ethanol and analysed; water was taken as the difference. Thickness came from the weights via Eq. 1 and, separately, from cross-sectional images; residence time is gel weight divided by total release rate. ······
- In situ imaging. A compact fused to a glass dish, its top sealed with a glass barrier, was submerged in buffer at 37 °C with manual pipette mixing, and its edge was imaged every 30 s with a 60× objective (230 nm resolution). Prodan marks the drug-rich (hydrophobic) phase blue, rhodamine 6G the water/polymer-rich (hydrophilic) phase red; magenta means both dyes are still mixed. The onset of phase separation was measured from the glass/gel boundary on the 3-7 min frames. ···
- Surface and cross-section. Compacts dissolved in the intrinsic apparatus for 2, 10 or 20 min were removed and imaged face-on at three scales, or cut in half and imaged in cross-section with z-stacks up to 200 μm. ·
- Hydrophobic phase. Compacts at 30% DL MePHPH and 5% DL PHPH, described as at the LoC of each system, were fully released in 10 mL buffer at 500 rpm; the nanoparticles were centrifuged at 21100 g, analysed by HPLC (dry basis) and, as wet pellets, by modulated DSC. ···
- Framework. A generic type I drug-polymer-water phase diagram was drawn with hydration paths, tie lines and the plait point, and three schematic cases were compared; nothing was computed. ···
Key equations
The gel volume is the sum of the drug, polymer and water volumes (weights w divided by densities ρ, with 1.25 g/mL for both drugs and 1.19 g/mL for PVPVA); dividing by the 0.5 cm² face gives the gravimetric thickness h in Table 2.·
Water enters the gel at a rate set by its diffusion coefficient D and its gradient across the gel; as the gel thickens the gradient flattens and penetration slows, until it matches the rate at which chains leave. Used only in words; as printed the equation is not dimensionally consistent.··
Terms used on this page
- Gel layer: the rubbery, swollen polymer layer between the dry glassy core (glass/gel interface) and the solution (gel/solution interface), where chains disentangle and leave.
- Residence time: how long one gel-layer thickness takes to dissolve away.
- Congruent release: drug and polymer leave at the same percent rate; incongruent: the drug lags or stops.
- Hydrophobic phase: the drug-rich phase formed when water splits the ASD; hydrophilic phase: the water- and polymer-rich phase.
- Segregative separation: the polymer goes to the hydrophilic phase. Associative separation: the polymer goes with the drug into the hydrophobic phase.
- Phase inversion: the minority phase becomes the continuous one.
- Plait point: the point of a ternary phase diagram where the two coexisting phases become identical; hydration path: the line of compositions a wetting ASD passes through.
03Main findings
Release collapses above about 40% DL for MePHPH and above 5% DL for PHPH
At 20 and 40% DL MePHPH, drug release at 30 min reached ≈96% and ≈61% against ≈53% for neat PVPVA; at 50% DL release lagged by more than 10 min and reached ≈15%, and at 70% DL nothing was released. For PHPH, 5% DL released ≈75% of the drug while 20% DL released nothing. ··
More detail
MePHPH compacts at 20% DL released drug and polymer together and faster than neat PVPVA (≈54 and ≈57% at 20 min, ≈96 and ≈105% at 30 min; neat PVPVA ≈40 and ≈53%). At 40% DL both still released at least as fast as neat PVPVA, but drug slightly lagged polymer by 30 min (≈61 versus ≈72%). At 50% DL both components showed a lag of more than 10 min and reached only ≈15% (drug) and ≈22% (polymer) at 30 min; at 70% DL no release was detected. ·· The 5% DL PHPH compact dissolved faster than neat PVPVA (drug ≈75%, polymer ≈83% at 30 min), while the 20% DL compact did not dissolve at all. In surface-normalized terms the total release rate was 4.4, 6.4 and 4.3 mg·min⁻¹·cm⁻² at 5, 20 and 40% DL MePHPH, 2.3 at 50% DL, zero at 70% DL, 5.5 for 5% DL PHPH and 3.7 for neat PVPVA. The authors call these results "as expected" from the LoCs of 40% and 5% DL reported earlier. · Percentages are calculated on a 100 mg compact weight, so values above 100% occur.
Drug piles up in the gel layer at 40 and 50% DL
Within 30 min the drug content of the gel (dry basis) rose from 40 to ≈49% at 40% DL and from 50 to ≈59.5% at 50% DL MePHPH, but stayed at the initial value for 20% DL MePHPH and 5% DL PHPH. The authors read this as the true MePHPH LoC lying below 40% DL ("This suggests"). ·
More detail
The gel drug content at 10, 20 and 30 min was ≈45, ≈46.5 and ≈49% at 40% DL and ≈52, ≈54.5 and ≈59.5% at 50% DL, the drug-polymer ratio climbing faster at 50% DL; at 20% DL MePHPH (≈19.8-20.8%) and 5% DL PHPH (≈5.0-5.1%) it did not change. The authors argue that this is a more sensitive test of congruency than separate release rates, because the drug accumulates in the gel while release is incongruent. They therefore place the true LoC below 40% DL, even though the earlier study reported at least 80% drug release at 40% DL. · Only 20, 40 and 50% DL were tested, so by this criterion the LoC lies between 20 and 40% DL. ·
Below the LoC the gel is thin and releases fast; above it the gel grows and dries out
Total release rate peaked at 20% DL MePHPH (6.4 against 3.7 mg·min⁻¹·cm⁻² for neat PVPVA), with the thinnest gel (140 μm by weight) and the shortest residence time (1.9 min). At 50% DL the gel was 334 μm thick, held 11% water and was still growing; at 70% DL it held 1.5% water. Water per polymer stayed between 0.25 and 0.41 except at 70% DL. ··
More detail
Gravimetric thickness was 258 μm for neat PVPVA, 227, 140, 189, 334 and 198 μm at 5, 20, 40, 50 and 70% DL MePHPH, and 356 and 586 μm at 5 and 20% DL PHPH; cross-sectional imaging gave similar values (251, 162, 171 at 30% DL, 233, 318 and 323 μm). · Water content fell with DL (25% for neat PVPVA, 18-19% at 5-40% DL MePHPH, 11% at 50%, 1.5% at 70%; 24 and 16% for 5 and 20% DL PHPH), while the water-to-polymer ratio stayed between 0.25 and 0.41 except at 70% DL (0.05). · For MePHPH the total release rate rose to a maximum at 20% DL, 70% faster than neat PVPVA, fell to about the neat PVPVA value at 40% DL and fell further above it; the residence time mirrored this (4.5, 1.9, 4.1 and 15 min at 5, 20, 40 and 50% DL; 5.7 min for neat PVPVA). · The 5% DL PHPH gel was about 40% thicker than the neat PVPVA gel ("somewhat surprising") yet released faster, so its residence time (5.3 min) matched that of neat PVPVA. ·· The 50% DL MePHPH and 20% DL PHPH gels had not reached steady state at 30 min; the authors attribute the thick 20% DL PHPH gel to water still entering while nothing leaves ("can be attributed"), and the near-dry 70% DL gel "likely" to water transfer blocked by a hydrophobic barrier. ·· They conclude that DL can change release rates both below and above the LoC ("These results indicate"). The printed residence times agree with the gel's drug-plus-polymer mass divided by the release rate rather than with its total weight.
MePHPH: droplets inside the gel up to 30% DL, networks at 40%, inversion at 50%
At 5, 20 and 30% DL, discrete drug-rich particles below 1 μm formed 155, 57 and 45 μm from the glass/gel boundary, less than the gel thickness measured in the release set-up (140-227 μm), and some were seen leaving into solution. At 40% DL some drug-rich domains connected into networks; at 50% DL the drug-rich phase became continuous within 60 s. ····
More detail
In every MePHPH gel the blue and red dyes separated, which the authors read as segregative phase separation into a drug-rich and a water-rich phase. · At 5, 20 and 30% DL the blue domains were discrete particles with diameters below 1 μm; phase separation began 155 ± 43, 57 ± 14 and 45 ± 20 μm from the glass/gel interface, moving closer to it as DL rose. Because these distances are shorter than the gel thickness from the release set-up, the authors conclude the nanoparticles form inside the gel ("suggesting"), and particles seen beyond the gel/solution interface show them being released ("indicating"). ·· At 40% DL some domains linked into networks in the image plane, continuous regions formed at times and intermittently ruptured, and the proportion of connected domains rose with DL ("visually apparent"). At 50% DL the morphology inverted by 60 s, with the drug-rich phase continuous and the water-rich phase as discrete pockets, and it persisted and coarsened up to 2100 s. ·· The in situ gel was mixed gently by pipette, so the authors caution that its size may not represent the release experiments; the inside/outside-gel conclusions compare two set-ups. ·
PHPH: particles form beyond the gel at 5% DL, and a network appears already at 10-20% DL
At 5% DL the drug-rich particles formed about 601 μm from the glass/gel boundary, beyond the 356 μm gel. At 10% DL the drug-rich phase was partly connected and at 20% DL fully connected, a loading at which MePHPH still gave droplets. Both dyes went into the PHPH drug-rich phase. ·····
More detail
In PHPH gels both dyes partitioned into the drug-rich phase, which stayed magenta, while the water-rich phase lost both dyes and looked black; the authors take this as a much less hydrophobic drug-rich phase, consistent with associative phase separation in which much polymer joins that phase ("This indicates"). · At 5% DL, sub-micrometre domains appeared 601 ± 68 μm from the glass/gel interface, beyond the 356 ± 18 μm gel, so the particles "appear to originate outside the gel layer". ··· At 10% DL the drug-rich phase was partly interconnected; in the 1800 s frame these domains lie beyond the marked gel/solution line. · At 20% DL the whole drug-rich phase was interconnected, with the water-rich phase as discrete pores in the image plane, whereas 20% DL MePHPH gave a discrete drug-rich phase. ·· The PHPH network deformed under the flow while the 40% and 50% DL MePHPH networks did not, suggesting a weaker network ("may have a lower mechanical strength"), in line with its lower Tg. · The onset distance moved closer to the glass/gel boundary as DL rose, as for MePHPH.
The PHPH drug-rich phase is three-quarters polymer and soft
The released hydrophobic phase of 5% DL PHPH contained 26.2 ± 0.5 wt% drug (dry basis) and had a Tg of −5.8 °C, against 98.8 ± 0.6 wt% drug and 16.8 °C for 30% DL MePHPH; both Tgs lie below 37 °C.
More detail
The MePHPH-rich phase was almost pure drug, and its onset Tg (16.8 ± 0.2 °C) was close to that of neat MePHPH (22.5 ± 0.1 °C); MePHPH, with a calculated log P of about 4, is "not expected" to absorb much water. ·· The PHPH-rich phase held about 75% PVPVA on a dry basis, and its Tg of −5.8 ± 0.6 °C was far below those of neat PHPH (84.5 °C) and PVPVA (101.3 °C), which the authors explain by water in the phase ("it is likely"); the water content of the pellet was not measured. ···· Both compositions resemble the equilibrated phases of the group's earlier study, which the authors take to mean the phases are mobile enough to reach equilibrium during dissolution ("suggesting"). ··
Above the LoC a porous drug-rich layer covers the surface
After 20 min the 50% DL MePHPH surface was largely a continuous drug-rich phase with water-rich pockets, and the cross-section showed a thick drug-rich layer on top; the 20% DL PHPH surface was porous. At 40% DL MePHPH only parts of the surface were continuous, and at 30% DL it stayed uniform with domains of about 1 μm. ····
More detail
On the surface, 30% DL MePHPH showed domains of about 1 μm or less, a few larger ones, and a uniform macroscopic view at 2 and 10 min. At 40% DL large interconnected domains at 2 min looked discrete at 20 min, but the macroscopic view was patchy, with continuous drug-rich regions next to discrete drug-rich domains in a continuous water-rich phase. At 50% DL continuous drug-rich domains covered a larger area and held discrete water-rich pockets, the inverse of 30% DL. · The 50% DL and 20% DL PHPH surfaces looked porous, as reported for ritonavir- and indomethacin-PVPVA and ritonavir-PVP ASDs. ··· The 5% DL PHPH surface was homogeneous and the 10% DL surface showed shades of magenta without features; the authors explain this by particles forming outside the gel and by smearing of the gel end on the glass ("likely"). ·· In cross-section, the 30% DL gel was macroscopically homogeneous; at 2 min the 40% DL gel was separated near the solution but homogeneous near the core, and the 50% DL gel separated at once and carried a thick drug-rich layer by 20 min. · Neat PHPH, MePHPH and PVPVA surfaces showed no phase separation, while 20% DL MePHPH did. ·
04Further observations
- Neat drug and polymer compacts never phase separate; a PVPVA gel forms with no separated domains. ·
- At 40% DL MePHPH the drug-rich network intermittently ruptured and covered only parts of the surface, yet release stayed good. ··
- The PHPH network deformed under flow; the MePHPH networks did not. ·
- At 2 min the 40% DL gel was separated only near the solution side.
- No crystallization was seen in any formulation (method not stated). ·
More detail
- Controls. Compact surfaces of neat PHPH, MePHPH and PVPVA stayed homogeneous after buffer exposure, and the in situ neat PVPVA compact formed a gel layer without separated domains; 20% DL MePHPH showed separated domains. ··
- The 40% DL borderline case. Continuous drug-rich regions formed on the compact at some time points and intermittently ruptured; the network appeared weaker than at 50% DL, which the authors explain by swelling pressure overcoming its strength ("A possible explanation"). Release was marginally faster than for neat PVPVA, but drug slightly lagged polymer and accumulated in the gel. ······ The authors expect the surface would become covered with time, hurting thicker compacts most ("may have a greater impact").
- Mechanical strength. The 20% DL PHPH network deformed under hydrodynamic stress; the 40% and 50% DL MePHPH networks did not. ···
- Gel profile. In cross-section at 2 min, the 40% DL gel was partly phase separated near the gel/solution interface but homogeneous near the glass/gel interface, which the authors read as too little water near the core ("may indicate"); by 20 min colour segregation was complete and the gel looked more homogeneous, "likely" from domains coalescing. The 50% DL gel separated immediately after forming, as expected for a higher DL. ···
- No crystallization. Crystallization was not observed in any formulation; the detection method is not described. The authors warn that drugs crystallizing faster than the gel residence time (about 5 min here) may lose congruent release. ··
- Image artefacts. Black regions in the gel came from pores or from light scattering by separated domains, and different shades of magenta in the dry compact from compression; the authors stress that the dark regions still contain drug, polymer and dyes. ·
05How the authors connect the findings
More detail
- Gel layer. PVPVA is a linear, nonionic, glassy, entangled polymer and dissolves through a rubbery gel layer. Water plasticizes the glass at the glass/gel interface; entangled chains there move slowly while their segments are mobile; the gel grows and swells as water enters and its viscosity falls; at a critical water content the chains disentangle and leave at the gel/solution interface. At steady state both interfaces move at the same rate, giving constant gel thickness and zero-order release from a flat face. A gel formed on every compact, so ASDs "may" dissolve like neat polymers. ··
- Drug leaves with the polymer. The drug is too poorly soluble to diffuse out of the gel, so its release is "solely" by polymer erosion, an assumption the authors call reasonable under the non-sink conditions used. Water drives amorphous phase separation; with MePHPH the polymer goes to the water-rich phase (segregative), with PHPH it joins the drug (associative). ···
Discrete drug-rich phase. The drug-rich phase forms nanoparticles inside the gel (5-30% DL MePHPH) that do not have time to coalesce in the viscous gel within the 2-6 min residence time ("It appears"), or the drug stays dissolved through the gel and separates in the diffusion layer or bulk (5% DL PHPH). In both cases the drug is "carried" out with the swelling and dissolving polymer.
Continuous drug-rich phase. Above the LoC both systems formed continuous or semi-continuous drug-rich phases. Being water-poor, the phase is "expected" to become more viscous; once connected it adds strength to the gel and, anchored in it, persists at the surface as an insoluble barrier. Its pores are first filled with water-rich phase, which lets some drug and polymer out just above the LoC and lets water reach the core, so the gel keeps growing (50% DL MePHPH, 20% DL PHPH); at 70% DL the pores shrink and the gel stays small ("may be because"). ···
What sets the switch point. Strong drug-polymer interactions, especially hydrogen bonding, help physical stability but can harm release in PVPVA ASDs; the low LoC of PHPH-PVPVA was attributed earlier to adhesive hydrogen bonding. Hydrogen bonding draws PVPVA into the drug-rich phase and makes it "volumetrically larger", so the network forms at lower DL; the conclusions state that the variation in LoC "was due to the extent of polymer present in the hydrophobic phase". ·
Conclusion drawn. In a type I drug-polymer-water diagram, a hydration path that enters the two-phase region right of the plait point passes through the drug-rich binodal, so the drug-rich phase is the majority and "intuitively" should form a network; entering left of it, the water-rich phase is the majority and the drug-rich phase stays discrete. The plait point therefore "serves as an arbiter for approximating the maximum LoC": associative systems have it to the left and a low maximum LoC, segregative systems to the right and a higher one, and a smaller miscibility gap also helps. This assumes near-equilibrium phase compositions along the hydration path, which "may" hold here because both drug-rich phases have Tg below 37 °C. ····
Release rate below the LoC. The rise in MePHPH release rate up to 20% DL "must be attributed" to faster water penetration and faster chain release: a thinner gel and plasticization of the dry polymer by MePHPH speed water entry ("may be explained"), and phase separation sends most water into the water-rich phase, so chains reach the disentanglement point sooner ("A possible explanation"). The fall above 20% DL "may be due" to MePHPH's lipophilicity lowering the driving force for water entry, and near the LoC to the barrier. The authors propose that the congruent release rate is controlled by water penetration and chain disentanglement. ····
06What it means for formulation
- Strong drug-polymer hydrogen bonding, good for stability, can lower the LoC of PVPVA ASDs. ··
- Thin tablets or small, well-dispersed ASD particles "may" release more completely near the LoC than compacts.
- For fast-crystallizing drugs, a polymer with a short gel residence time "may be worthwhile".
- Gel drug content over time can flag incongruent release before percent release looks bad.
- Near the LoC, a 30 min compact test can look fine while a drug-rich network is already forming.
More detail
- Strong drug-polymer interactions, particularly hydrogen bonding, improve physical stability but can be detrimental to release, especially in PVPVA ASDs; the study "highlights the importance of drug-polymer interactions" for release as a function of DL. ··
- Thinner tablets or small, well-dispersed ASD particles "may have more complete drug release" near the LoC than compacts, though this "may be challenging" in tablets, which can disintegrate poorly at moderate-to-high ASD loads.
- Drugs whose crystallization induction time is shorter than the gel residence time (about 5 min here) may crystallize in the gel and lose congruent release; if this cannot be inhibited, "it may be worthwhile" to choose a polymer with a short gel residence time.
- Modelling drug-polymer-water phase diagrams could "potentially" turn the framework into quantitative LoC predictions for in silico formulation design.
- Gel-layer drug content is a cheap readout: at 40% DL MePHPH it rose while percent release still beat neat PVPVA, so it may catch an LoC that release curves miss.
- A 30 min compact test near the LoC can be optimistic: at 40% DL the network was already present in patches, and the authors expect it to cover the surface over longer times or in thicker tablets.
- In this picture what matters is how much polymer the drug-rich phase carries, not drug hydrophobicity alone; excipients or polymers that keep the polymer out of that phase would be expected to raise the LoC, which this paper did not test.
07Open questions
- How do ASDs with high-Tg drug-rich phases, which may not reach near-equilibrium, behave?
- Can modelled ternary phase diagrams give quantitative LoC predictions?
- No phase diagram of either system was measured or computed, so the plait-point rule is untested here.
- Composition was measured at one DL per drug, from particles released in bulk rather than from the gel.
More detail
- Additional work is needed to understand the behaviour and impact of high-Tg hydrophobic phases, for which the near-equilibrium assumption may fail.
- Thicker compacts or longer times near the LoC may let a partial network cover the surface and hinder release.
- The kinetic-thermodynamic relationships could be developed into quantitative LoC predictions by modelling ternary phase diagrams.
- No phase diagram, plait point or hydration path of the two systems was measured or computed; the framework rests on schematic diagrams.
- The hydrophobic-phase composition was measured once per drug, at different DLs, on nanoparticles released in bulk at 500 rpm, not on the gel-layer phase at the PHPH network loadings.
- Transport through the network was not measured, and release and imaging were run under different stirring. ·
- Hydrogen bonding and water content in the hydrated phases, which carry the explanation, were not measured. ·
- Only two closely related drugs, one polymer and compacts were studied.
08How solid
AI assessment, not a statement made in the paperRelease, gel drug content and three imaging modes agree on where morphology and release change for both drugs. But the barrier and polymer-content explanations rest on co-occurrence across experiments run under different stirring, one composition per drug and cited work, and the phase-diagram framework is schematic. ······
More detail
- For both drugs, the loading at which the drug-rich phase connects matches the loading at which release fails (MePHPH 40-50% DL, PHPH 10-20% DL). ···
- The morphology change is seen in situ, on the surface and in cross-section. ··
- Gel attributes are quantitative with standard deviations, and gel drug accumulation gives an independent sign of incongruence. ·
- The composition contrast of the drug-rich phases is large (98.8 versus 26.2 wt% drug).
- The barrier is inferred: release and morphology come from separate experiments, and at 40% DL a partial network coexisted with good release. ·
- Inside-versus-outside-gel conclusions compare in situ onset distances with gel thicknesses from a differently stirred set-up.
- The polymer-content explanation rests on one composition per drug at different DLs, from particles released in bulk.
- The MePHPH LoC is stated as 40% DL, "at" 30% DL and "below 40%" in different places. ·
- No phase diagram underlies the plait-point framework.
- Several captions and figures disagree with the text (Fig. 10 colour key, Fig. 15 versus Table 2, a wrong SI figure cited), and the residence times match dry rather than total gel mass. ···
09Figure guide
Every figure and table of the paper, what it is there for, and what to check on the original. Key figures are shown with the story.
| Figure | What it does in the paper | Supports | Check (AI note) |
|---|---|---|---|
| Graphical abstract (p.2217) | Pictures the three surface phenomena: gel, nanoparticles, network. | header | A schematic, not data. |
| Fig. 1 (p.2218) | Defines the systems: PHPH with two OH groups, MePHPH with both methylated, PVPVA and the two dyes.···· | 0.2 | The caption labels rhodamine 6G "(c)"; it is panel (e). |
| Table 1 (p.2219) | HPLC settings for drug and polymer quantification. | 0.2 | Flow-rate unit printed as μL·min⁻¹. |
| Fig. 2 (p.2220) | Shows the three confocal set-ups: in situ edge, surface after removal, cross-section.·· | 0.2 | A schematic, not data. |
| Fig. 3 (p.2221)key figure | The release cliff for both drugs and neat PVPVA.· | F1, K1 | Percent release on a 100 mg basis; values above 100% occur. |
| Fig. 4 (p.2221)key figure | Drug accumulation in the gel at 40 and 50% DL MePHPH only. | F2, K2 | Only 20, 40 and 50% DL MePHPH tested. |
| Table 2 (p.2222)key figure | Gel thickness, water, release rate and residence time for all compacts. | F3, K5 | Residence times match dry, not total, gel mass. |
| Fig. 5 (p.2223)key figure | 30% DL MePHPH: discrete droplets form inside the gel and leave into solution. | F4, K3 | |
| Fig. 6 (p.2224)key figure | 40% DL MePHPH: domains start to connect into networks. | F4 | |
| Fig. 7 (p.2225)key figure | 50% DL MePHPH: inverted, continuous drug-rich phase. | F4, K1 | |
| Fig. 8 (p.2226)key figure | 5% DL PHPH: particles form beyond the gel. | F5, K3 | Onset compared with a gel thickness from another set-up. |
| Fig. 9 (p.2227) | 10% DL PHPH: partly connected drug-rich phase. | F5 | The domains lie beyond the marked gel/solution line. |
| Fig. 10 (p.2228)key figure | 20% DL PHPH: fully connected magenta network. | F5, K4 | The caption colour key is reversed. |
| Table 3 (p.2228)key figure | Tg and dry-basis drug content of the released drug-rich phase. | F6, K4 | Pellet water content not measured. |
| Fig. 11 (p.2229)key figure | MePHPH surfaces: uniform at 30%, patchy at 40%, continuous at 50% DL. | F7, K1 | |
| Fig. 12 (p.2229)key figure | PHPH surfaces: homogeneous at 5%, porous at 20% DL. | F7 | |
| Fig. 13 (p.2230)key figure | MePHPH cross-sections: gel structure and the thick layer at 50% DL. | F7 | |
| Fig. 14 (p.2230)key figure | Schematic of polymer dissolution through a gel layer. | 0.5 | A schematic, not data. |
| Fig. 15 (p.2230)key figure | Onset of phase separation against the gel/solution boundary. | F4, K3 | The 30% DL boundary differs from Table 2. |
| Fig. 16 (p.2231) | Illustration: MePHPH-rich nanoparticles in a hydrophilic phase like the neat PVPVA gel. | 0.5 | A schematic, not data. |
| Fig. 17 (p.2232)key figure | Generic type I diagram with congruent and incongruent hydration paths.· | 0.5, K6 | A schematic, not data. |
| Fig. 18 (p.2232)key figure | Plait point position and maximum LoC for three schematic cases. | 0.5, K6 | A schematic, not data. |