Does SDS speed up atazanavir crystallization from supersaturated solution through its single molecules or through its micelles, and does it undo the crystallization inhibition of common ASD polymers?
Through sub-micellar SDS, not micelles: at constant supersaturation the induction time stayed near 200 min up to 0.05 mg/mL SDS, fell to about 50-60 min by 0.3 mg/mL and fell no further above the CMC of 0.5 mg/mL. · With 0.1 mg/mL SDS, PVPVA held off crystallization for about 350 min instead of more than 1000, while HPMC-606 and HPMCAS-MF still held for more than 1000 min.
For atazanavir at 37 °C in pH 6.8 phosphate buffer, dosed in each medium at its own amorphous solubility (SRamorph stated as ~65), SDS shortened the nucleation induction time only above a threshold between 0.05 and 0.075 mg/mL, far below its cited CMC of 0.5 mg/mL, and micellar SDS gave no further shortening. ···· The authors read the threshold as a critical hemimicelle concentration: pyrene in ATZ crystal slurries sensed a more hydrophobic, crowded environment over the same range, and they propose that SDS hemimicelles on the nucleus or crystal surface lower the crystal-water interfacial energy (abstract: "strongly suggest"; discussion: "is hypothesized"). ··· With 1 mg/mL polymer and 0.1 mg/mL SDS, PVPVA lost part of its inhibition while HPMC-606 and HPMCAS-MF kept theirs for at least 1000 min; PVPVA also brought SDS aggregation forward more (CAC 0.1 versus 0.2 mg/mL), and the authors attribute its loss "most likely" to SDS binding PVPVA in solution so that less polymer reaches the crystal surface. ···· SDS adsorption on ATZ, the interfacial energy and polymer adsorption were not measured, and the induction time does not separate nucleation from growth to a detectable size. ····
01Why this study
PVPVA, HPMC and HPMCAS slow nucleation and growth from supersaturated solution, thought to depend on how the polymer binds the nucleus and adsorbs on the crystal.
Formulation surfactants have been seen to induce or inhibit crystallization; promotion is believed to come from a lower crystal-solution interfacial energy.
Rodríguez-Hornedo 2004, ref 22; König 1988, ref 52 ·
Micellar surfactant acts only if it first releases monomers.
Canselier 1993, ref 29; Dugua 1978, ref 56
It may bind the polymer in solution and keep it off the crystal.
Ziller 1988, ref 25; Ilevbare 2012, ref 63
Concentration ratios mislead in SDS solutions, so the group measured ATZ supersaturation by membrane flux.
Indulkar 2017, ref 64
More detail
The references are numbered in the paper; ref N below is the printed number.
What was already known. The introduction builds on these points:
- Supersaturation is the benefit, crystallization the risk. ASDs and other supersaturating formulations give concentrations far above the crystalline solubility and, at equal total concentration, a higher membrane flux than micellar or cyclodextrin solubilization (Raina 2015, ref 9). Above the amorphous solubility, liquid-liquid or glass-liquid phase separation gives drug-rich nanodroplets that keep the flux at its maximum for longer (Indulkar 2016, ref 14) and raised bioavailability in rats for itraconazole and enzalutamide (refs 15, 16). Supersaturated solutions are metastable, so crystallization is always possible (refs 17-20). ···
- Additives act at the crystal surface. Adsorbed additives change thermodynamic factors (interfacial energy, step curvature through step pinning) and kinetic factors (blocking kink sites) (refs 24-31). PVPVA, HPMC and HPMCAS inhibit both nucleation and growth (refs 32-36); their effect is thought to depend on binding the drug aggregates that form the nucleus and on adsorbing on the growing crystal, through hydrophobic, hydrogen-bonding or ionic interactions (refs 25, 37-42); HPMCAS inhibits felodipine growth better in an extended than a globular adsorbed conformation (Schram 2014, ref 37). Some polymers instead induce crystallization (refs 43, 44). ··
- Surfactants are less predictable. They improve wetting and dissolution (ref 45), and bile salts and phospholipids are present in intestinal fluids. Bile salts have consistently inhibited crystallization (Chen 2015, ref 47; refs 46, 48), while formulation surfactants have both induced and inhibited it, by adsorbing at the crystal-water interface and sometimes changing habit (refs 22, 27, 51-54). Polymeric surfactants may promote crystallization through self-association.
- How surfactants could promote nucleation. Promotion is believed to come from a lower interfacial energy at the crystal-solution interface (refs 52, 55, 56); additives can also change the pre-exponential kinetic factor of nucleation theory and solute solvation or desolvation (refs 57-59).
- Which form of the surfactant acts. Monomers are thought to adsorb on the growing nucleus (Canselier 1993, ref 29); molecules in micelles act only if they leave the micelle and adsorb as monomers, which requires adsorption to be more favourable than micellization (Dugua 1978, ref 56). Amphiphile layers at the air-water surface (refs 60-62), nuclei stabilized inside micelle cores (ref 29) and particles adsorbed on micelles (ref 54) have also been reported.
- Three outcomes for an inhibiting polymer plus an accelerating surfactant. The polymer adsorbs strongly and keeps the surfactant off; the surfactant adsorbs strongly and counteracts the polymer; or the surfactant binds the polymer in solution and stops it adsorbing (Ziller 1988, ref 25; Ilevbare 2012, ref 63).
- The ATZ-SDS system was characterized before. The CMC of SDS in 50 mM pH 6.8 phosphate buffer is 0.5 mg/mL, and supersaturation in micellar media must be judged by activity rather than concentration (Indulkar 2017, ref 64). ·
What the paper set out to do. Measure the induction time of ATZ from supersaturated solution at one supersaturation over SDS concentrations from well below to well above the CMC, to separate the roles of monomeric and micellar SDS; probe the mechanism with pyrene fluorescence on ATZ crystal slurries; and test whether SDS changes the inhibition by three ASD polymers at concentrations typical of ASD dissolution. ···
02How they approached it
One drug and one surfactant: ATZ in pH 6.8 buffer at 37 °C, dosed in every SDS medium at that medium's own amorphous solubility, so the supersaturation stays the same (SRamorph ~65) while SDS rises from 0 to 3.6 mg/mL, across the cited CMC of 0.5 mg/mL. The polymer tests use 1 mg/mL polymer and 0.1 mg/mL SDS, meant to mimic ASD dissolution. ····
What was done
Crystalline (48 h equilibration) and amorphous (scattering onset) solubility of ATZ in 0-3.6 mg/mL SDS.··
Diffusion-cell flux at the amorphous and crystalline solubility→SRamorph ~65 in all media.··
ATZ at its amorphous solubility in 13 SDS levels→extinction→induction time.·
1 mg/mL PVPVA, HPMC-606 or HPMCAS-MF with or without 0.1 mg/mL SDS→induction time.·
6:85.5:8.5 ATZ:PVPVA:SDS ASD dissolved→induction time.··
ATZ crystal slurries below the CMC + pyrene→I1/I3 and excimer emission.··
Pyrene in 1 mg/mL polymer solutions→CAC of SDS.·
Microscopy and NTA→crystal size and habit.···
Induction-time regions set against the fluorescence change (crystal slurries) and the CAC ranking (polymers).···
More detail
What was done
- Solubility. Excess crystalline ATZ was equilibrated for 48 h at 37 °C in buffer or SDS solution, ultracentrifuged at 35000 rpm and assayed by HPLC (C18 column, UV 210 nm). Amorphous solubility was the ATZ concentration at which a fibre-optic probe first saw scattering while a 30 mg/mL methanolic stock was infused into the stirred medium, each run finishing within 10 min. ·
- Supersaturation. ATZ was dosed into the donor of a side-by-side diffusion cell (7.07 cm² regenerated cellulose membrane, 6-8 kD cut-off, 34 mL per side, 37 °C) at the amorphous or the crystalline solubility; the receiver was sampled by HPLC and the flux taken from the slope of mass per area against time. The flux ratio gives SRamorph. Flux values and the SDS levels tested are not printed. ··
- Induction time. 20 mL of medium at 300 rpm and 37 °C received ATZ from the stock at the amorphous solubility of that medium, with methanol held at about 4.5% v/v in every run. Extinction at a non-absorbing wavelength was read every minute; the induction time is the first rise above baseline noise, and so includes both the time to form nuclei and the time to grow them to a detectable size. Thirteen SDS levels from 0 to 3.6 mg/mL were run; replicates are not stated. ··
- Polymers. The same test in 1 mg/mL PVPVA, HPMC-606 or HPMCAS-MF, with or without 100 µg/mL SDS. A 6:85.5:8.5 ATZ:PVPVA:SDS dispersion made by rotary evaporation from methanol (150-250 µm) was also dissolved, 23.5 mg in 20 mL, to the same final concentrations, with no methanol stock. ··
- Fluorescence on crystal slurries. ATZ was crystallized almost to completion from its amorphous solubility in SDS solutions below the CMC (0-0.3 mg/mL), pyrene was added to 0.4 µg/mL, and its emission (excitation 332 nm) was read for the I1/I3 ratio and for excimer emission between 450 and 550 nm.
- CAC. The same pyrene readout in 1 mg/mL polymer solutions without ATZ, with SDS from 0.01 to 0.5 mg/mL; the CAC is the SDS level above which I1/I3 falls steadily.
- Crystal size. Crystals formed at each SDS level were sized by polarized light microscopy below 75 µg/mL SDS and by NTA (Stokes-Einstein, 532 nm laser) above.
Key equations
Supersaturation is the activity a of the dissolved drug relative to its activity a* at the crystalline solubility. Flux across a membrane is proportional to activity, with diffusion coefficient D, membrane thickness h and the drug's activity coefficient in the membrane γm held constant, so the ratio of the flux at the amorphous solubility to the flux at the crystalline solubility gives SRamorph without needing to know how much drug sits in micelles.··
The flux is the mass dm crossing area A in time dt, taken as the slope of transferred mass per area against time.
The measured time is the sum of the time to form the first nuclei and the time for them to grow large enough to scatter; an additive can act on either.·
Terms used on this page
- Nucleation induction time (NIT): time from making the supersaturated solution until crystals are first detected, here by light extinction.
- SRamorph: the supersaturation ratio of a solution at the amorphous solubility, judged by activity (flux), not concentration.
- Critical micelle concentration (CMC): the surfactant concentration above which micelles form in bulk solution.
- Hemimicelle (admicelle): a surfactant aggregate adsorbed on a surface below the CMC; the critical hemimicelle concentration (CHMC) is where such aggregates first form.
- Critical aggregation concentration (CAC): the surfactant concentration at which aggregates first form on dissolved polymer chains, below the CMC.
- Pyrene I1/I3: the ratio of the first to the third emission peak of pyrene; high (about 1.85 here) in water, lower in a hydrophobic environment. Excimer: an excited pyrene pair that emits broadly near 450-550 nm, formed only when pyrene molecules sit a few ångströms apart.
- NTA: nanoparticle tracking analysis; sizes particles from their Brownian motion in a video.
03Main findings
Solubility is flat up to the CMC and climbs above it; supersaturation is the same in every medium
Crystalline solubility stayed near 1.1 µg/mL and amorphous solubility near 70 µg/mL up to 0.3 mg/mL SDS; above the CMC both rose, to about 46 and 1480 µg/mL at 3.6 mg/mL. SRamorph was stated as ~65 in all media. ·
More detail
Without SDS, ATZ had a crystalline solubility of 1.1 µg/mL and an amorphous solubility of 70 µg/mL in 50 mM pH 6.8 phosphate buffer at 37 °C. Neither changed noticeably up to 0.3 mg/mL SDS (read from Fig. 2: about 1.1 and 70-80 µg/mL). From the CMC upwards both rose with SDS, which the authors assign to micellar solubilization: crystalline about 6.1, 7.9, 16.7, 22.3, 33.6 and 46 µg/mL and amorphous about 230, 300, 480, 820, 1180 and 1480 µg/mL at 0.8, 1, 1.5, 2, 3 and 3.6 mg/mL (plot readings). · Because every NIT run was dosed at the amorphous solubility of its own medium, the flux-based supersaturation SRamorph was ~65 in buffer and in the SDS media, so the NIT comparisons are at constant supersaturation. ·· The flux values behind this and the SDS levels tested are not printed; concentration ratios read from Fig. 2 are about 64 without SDS but about 35-38 above the CMC, which the paper does not discuss.
SDS shortens the induction time only above a threshold, and the effect stops at the CMC
The NIT was about 200 min up to 0.05 mg/mL SDS (region I), fell to about 56 min at 0.3 mg/mL (region II), and stayed at about 50-70 min from 0.5 to 3.6 mg/mL (region III).
More detail
At SRamorph ~65 the induction time without SDS was about 200 min. Read from Fig. 3, it stayed at about 199-216 min at 0.01, 0.025 and 0.05 mg/mL SDS (region I), then fell to about 177, 134, 101, 74 and 56 min at 0.075, 0.1, 0.15, 0.2 and 0.3 mg/mL (region II), and was about 53, 68, 66 and 52 min at 0.5, 1, 2 and 3.6 mg/mL (region III). The authors summarise this as no effect below 0.075 mg/mL ("does not seem to impact"), shortening from ~200 to ~50 min between 0.075 and 0.5 mg/mL where SDS exists as monomers, and no change above 0.5 mg/mL "even though the SDS concentration is greatly increased". ·· They state that a minimum of 0.075 mg/mL is needed, as Michaels and Tausch saw for SDBS and adipic acid growth, and that, because micelles add nothing, crystallization "appears to be induced by monomeric SDS molecules", as Shor saw for potassium nitrate nucleation up to the CMC. · The threshold is given in mixed ways: 0.05 mg/mL is the last unaffected level and 0.075 mg/mL the first with a shorter NIT; the region I error bars are wide (about ±25 to ±56 min). ·
Pyrene in ATZ crystal slurries senses SDS aggregates over the same range
I1/I3 stayed at about 1.85 up to 0.05 mg/mL SDS and fell to about 1.82, 1.79 and 1.68 at 0.1, 0.2 and 0.3 mg/mL; excimer emission appeared faintly at 0.1 and clearly at 0.2-0.3 mg/mL. ·
More detail
In slurries of ATZ crystals grown in SDS below the CMC, pyrene I1/I3 was about 1.85 in neat buffer and at 0.025 and 0.05 mg/mL SDS, which the authors give as similar to buffer without ATZ and SDS (value not shown). It then fell to about 1.82 at 0.1, 1.79 at 0.2 and 1.68 at 0.3 mg/mL; two lines drawn on the figure meet near "~0.075 mg/mL". The excimer region showed no peak up to 0.05 mg/mL, a "subtle" rise at 0.1 mg/mL and a broad maximum near 465-475 nm at 0.2 and 0.3 mg/mL. The authors read the lower I1/I3 as a more hydrophobic environment and the excimer as pyrene molecules close together, that is, aggregated SDS structures below the CMC ("suggests", "indicating"), which they place on the ATZ surface as hemimicelles; since the solutions are below the CMC, they exclude micelles in buffer. ··· No pyrene run in the same SDS solutions without crystals is reported, and the slurries contain very different crystal sizes on either side of the threshold. ·
SDS weakens PVPVA as an inhibitor but not HPMC-606 or HPMCAS-MF
Alone, each polymer held off crystallization for more than 1000 min. With 0.1 mg/mL SDS (NIT 130 min without polymer), PVPVA held for about 350 min, while HPMC-606 and HPMCAS-MF still held for more than 1000 min.
More detail
At 1 mg/mL, PVPVA, HPMC-606 and HPMCAS-MF each prevented detectable crystallization for at least 1000 min at SRamorph. With 0.1 mg/mL SDS, which alone shortened the NIT to 130 min (about 135 min in Fig. 4), the NIT with PVPVA was 350 min, while both cellulosic polymers still exceeded 1000 min. · The authors describe PVPVA's loss as "to some extent" in the results, "substantially reduced (from 1000 to 350 min)" in the discussion and "lost some of its inhibitory effect" in the abstract; the cellulosics were unaffected "at least for the experimental duration studied". Only one SDS level was tested, and the no-SDS polymer values are censored at 1000 min.
PVPVA brings SDS aggregation forward more than the cellulosic polymers
In 1 mg/mL polymer solution SDS began to aggregate at 0.1 mg/mL with PVPVA and 0.2 mg/mL with HPMC-606 or HPMCAS-MF, against a CMC of 0.5 mg/mL without polymer. ·
More detail
Pyrene I1/I3 in polymer solutions without ATZ gave a CAC of 0.1 mg/mL SDS with PVPVA and 0.2 mg/mL with each cellulosic polymer; the titration curves are not shown. The authors read this through the necklace (bead-on-a-string) model, in which SDS aggregates form on the polymer chain below the CMC: all three polymers interact with SDS, and PVPVA more strongly ("suggesting"). · They state that the extent of surfactant-polymer interaction "was found to correlate" with the NIT change. The test SDS level of 0.1 mg/mL equals the PVPVA CAC and is below the cellulosic CAC.
04Further observations
- SDS turns 25-100 µm crystal agglomerates into crystals of about 130-370 nm. ·
- Dissolving the ATZ:PVPVA:SDS ASD gave an NIT of about 300 min, close to the 350 min from the stock solution. ·
- Above the CMC the NIT did not fall further although the amorphous solubility rose more than tenfold. ·
More detail
- Crystal size. At SDS levels of region I the crystals formed 25-100 µm agglomerates (polarized light image at 0.025 mg/mL). From 0.075 mg/mL, NTA saw sub-micron particles, described as needle-shaped and scattering anisotropically (frame at 0.3 mg/mL), with sizes of about 367 nm at 0.075 mg/mL and about 127-249 nm from 0.1 to 3.6 mg/mL (Fig. 7, plot readings). ·· The authors attribute the small size to adsorbed SDS whose charged head group prevents agglomeration. The text's bound of ≤ 350 nm does not fit the 0.075 mg/mL bar, and the needle shape rests on one NTA frame. ·
- ASD dissolution. The 6:85.5:8.5 ATZ:PVPVA:SDS dispersion dissolved to 70 µg/mL ATZ, 1 mg/mL PVPVA and 0.1 mg/mL SDS gave an NIT of ~300 min, "in line with" the 350 min from the methanolic stock. The authors conclude the solid particles did not seed nucleation, "possibly" because the ASD dissolves faster than ATZ crystallizes and/or the polymer inhibits heterogeneous nucleation. ··· The ASD run had no methanol; the stock runs had about 4.5% v/v.
- Solubilization without further acceleration. Between 0.5 and 3.6 mg/mL SDS the amorphous solubility rose from about 115 to 1480 µg/mL (and the ATZ dose with it), yet the NIT stayed at about 52-68 min. ·
05How the authors connect the findings
More detail
- SDS has a hydrophobic chain that drives micellization and a charged head group that opposes it. At low concentration it is dissolved as monomers; up to 0.05 mg/mL, neither the NIT nor the pyrene signal changes. ··
- Monomers can adsorb on surfaces such as ATZ nuclei or small crystals with the tail on the crystal. Based on Fig. 5 the adsorption "appears to become significant" above 0.075 mg/mL, and the adsorbed molecules can organize as hemimicelles (Fig. 8), a known form of surfactant adsorption below the CMC whose density rises up to the CMC. The authors place the CHMC of SDS on ATZ "around 0.05 mg/mL" from the NIT data, a "supposition" supported by the fluorescence, and in the conclusions state that the critical concentration "corresponds" to where hemimicelle formation is first observed. ···
- Adsorbed hemimicelles can reduce the interfacial energy at the crystal-solution interface, "potentially" promoting nucleation and/or growth; "this mechanism is hypothesized to play a role". The pyrene data are read as a hydrophobic, confined environment "as would be expected" in a hemimicelle. The authors add that additives can also change the pre-exponential factor and solvation of the nucleus. ··
- Above the CMC, adding SDS no longer shortens the NIT. The authors attribute this to SDS forming and remaining in micelles, which with their charged hydrophilic surface "cannot possibly adsorb" onto the hydrophobic nucleus; only hemimicelles can. Since micelles do not enhance nucleation, "it can be safely concluded" that crystallization does not occur inside micelles. ·
Cellulosic polymers. SDS interacts with HPMC-606 and HPMCAS-MF too (CAC 0.2 mg/mL), but less strongly; "we can speculate" that their strong adsorption to the drug keeps SDS off the emerging crystal surface, so the NIT stays above 1000 min. ··
PVPVA. SDS forms aggregates on PVPVA chains from 0.1 mg/mL (necklace model). This "appears highly favorable" and "may reduce" the polymer available to adsorb on the crystal surface, lowering its inhibition (350 min instead of more than 1000); in the conclusions the stronger interaction "most likely" reduces the polymer available for nascent crystal surfaces. ···
What sets the switch point. Whether a polymer keeps working with a surfactant depends on the balance between the affinity of the surfactant for the polymer and that of the polymer for the crystal surface.
Conclusion drawn. The conclusions state that the mechanisms "have been elucidated": SDS promotes crystallization only above a critical concentration far below its CMC that corresponds to hemimicelle formation, and the extent of surfactant-polymer interaction "was found to correlate" with the NIT change. ··
06What it means for formulation
- Surfactants added for dissolution can trigger crystallization; keep the surfactant below the level that does so while still helping dissolution. ·
- Check each polymer with and without the surfactant before choosing the pair. ·
- "Below the CMC" is not a safe surfactant level: for ATZ the effect starts at about a tenth of the CMC.
- With SDS present, the cellulosic polymers kept their protection here and PVPVA did not.
More detail
- Surfactants chosen to enhance dissolution "can induce crystallization" of the drug on supersaturation, which can negate the benefit of the supersaturating formulation.
- Since a minimum surfactant concentration is needed to promote crystallization, a product "can be formulated" with the surfactant minimized to a level that enhances dissolution but not crystallization.
- Polymers that normally inhibit crystallization "may or may not be effective" with surfactants, depending on the balance of surfactant-polymer and polymer-crystal affinities, so the combination can affect in vivo performance; knowing a polymer's effectiveness with and without surfactant "can aid" rational selection. ··
- For ATZ the shortening began between 0.05 and 0.075 mg/mL SDS, about 10-15% of the CMC. A surfactant level chosen only to stay below the CMC can therefore already sit in the accelerating range.
- The tested ASD composition (8.5% SDS with 6% drug) put 0.1 mg/mL SDS in solution at the drug's amorphous solubility, inside that range. The surfactant-to-drug ratio, not only the surfactant loading, decides where a dissolving ASD lands.
- In this system HPMC-606 and HPMCAS-MF kept their protection with SDS and PVPVA lost most of it, and PVPVA also had the lowest CAC. A CAC test of the candidate polymer with the intended surfactant may be a cheap first screen, though here it rests on one drug, three polymers and one SDS level.
- Above the CMC, extra SDS raised the amorphous solubility more than tenfold without shortening the induction time further, so the accelerating range lies below the CMC, not above it.
07Open questions
- Additives may also act through the pre-exponential factor and nucleus solvation, not only interfacial energy.
- Induction time covers nucleation and growth; both should be considered.
- SDS adsorption on ATZ and the interfacial energy were not measured.
- No pyrene control without crystals; the slurries differ in crystal size. ·
More detail
- Besides lowering the interfacial energy, additives can change the pre-exponential kinetic factor (solute diffusivity) and solvation or desolvation of the nucleus.
- The NIT includes both the formation of critical nuclei and their growth to a detectable size, so additive effects on both processes should be considered.
- The amount and structure of SDS adsorbed on ATZ, and the change in interfacial energy, were not measured; the hemimicelle reading rests on pyrene in slurries. ·
- Pyrene in the same SDS solutions without ATZ crystals, the needed control, is not reported, and the low- and high-SDS slurries contain crystals of very different size. ·
- Nucleation and growth were not separated, although crystal size changed with SDS.
- Polymer adsorption on ATZ, with and without SDS, was not measured; the polymer comparison used one SDS level and was censored at 1000 min. ·
- Equal supersaturation in all SDS media is stated without the flux data.
- One drug, one surfactant, about 4.5% methanol in all solution runs, no bile salts or other surfactants.
08How solid
AI assessment, not a statement made in the paperThe induction-time pattern (no effect, a drop, a plateau at the CMC) is clear and lines up with the pyrene change. The hemimicelle mechanism and the PVPVA explanation are indirect, key controls and replicate numbers are missing, and the polymer comparison rests on one SDS level. ····
More detail
- The three-region NIT pattern spans 13 SDS levels at constant supersaturation, and the region II fall (about 200 to 56 min) is larger than the error bars. ·
- The pyrene I1/I3 change and the excimer appear over the same SDS range as the NIT drop, and below the cited CMC. ·
- The plateau above the CMC holds although the amorphous solubility rises more than tenfold. ·
- PVPVA versus cellulosics with SDS is a large difference (350 versus more than 1000 min), and the ASD run reproduced the PVPVA result without methanol. ·
- No pyrene control without crystals; the CMC is cited, not measured under the slurry conditions; crystal size changes across the same threshold. ·
- The NIT mixes nucleation and growth to detection; the "nucleation rate" wording goes beyond it.
- Equal SR across SDS media is stated without flux data.
- The polymer ranking rests on two CAC values and one SDS level, with NITs censored at 1000 min.
- Replicates and error-bar meaning are not stated; the threshold and the top SDS level are given inconsistently; the size bound in the text does not fit the figure. ···
- The mechanism claims about micelles (no adsorption, no nucleation inside) rest only on the NIT plateau.
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) |
|---|---|---|---|
| Fig. 1 (p.19)key figure | Defines the materials: atazanavir, SDS and the three polymers.·· | 0.2 | |
| Fig. 2 (p.20)key figure | Shows solubility unchanged up to the CMC and rising above it, so each medium's dose can be set at its amorphous solubility. | F1 | Categorical x-axis; concentration ratios change with SDS.· |
| Fig. 3 (p.21)key figure | The central result: NIT unchanged in region I, falling in region II, flat in region III. | F2, K1, K2 | Threshold stated as 0.05 or 0.075 mg/mL; top level 3.6, not 3 mg/mL.· |
| Fig. 4 (p.22)key figure | Shows SDS cutting PVPVA's protection to about 350 min while the cellulosics stay above 1000 min. | F4, K5 | One SDS level; values censored at 1000 min. |
| Fig. 5 (p.23)key figure | The mechanistic evidence: I1/I3 falls and excimer emission appears over the same range as the NIT drop.· | F3, K3, K4 | No control without crystals; crystal size differs across the range.· |
| Fig. 6 (p.24) | Shows crystal habit: agglomerates at 0.025 mg/mL SDS, sub-micron elongated particles by NTA at 0.3 mg/mL.· | 0.4 | Needle shape rests on this NTA frame only. |
| Fig. 7 (p.24)key figure | Gives crystal sizes of about 127-367 nm from 0.075 to 3.6 mg/mL SDS. | 0.4 | 0.075 mg/mL bar exceeds the 350 nm stated in the text. |
| Fig. 8 (p.25)key figure | Illustrates the proposed SDS states: monomers, hemimicelles on ATZ, micelles in bulk.· | 0.5 | A schematic, not data. |
| Graphical abstract (p.26) | Summarizes the NIT results with idealized bars and cartoons.· | header | A schematic, not data. |