Dapsone: the monograph

Dapsone is 4,4'-diaminodiphenyl sulfone (DDS), a synthetic sulfone: molecular formula C12H12N2O2S, molecular weight 248.30, a white to slightly yellow-white crystalline powder ^11,1. Its antimicrobial activity was discovered in 1937, in the middle of the sulfonamide era, and the molecule turned out to have two separable talents: it kills or suppresses certain bacteria, and it quiets neutrophil-driven inflammation the way an NSAID quiets prostaglandin-driven inflammation ²⁸.

That dual nature produced two entirely different medical lives. As an oral tablet, dapsone spent more than 60 years as a systemic drug for serious disease: it is the label-recognized primary treatment for dermatitis herpetiformis and a pillar of leprosy multidrug therapy, with a real, dose-related hematologic cost that demands blood-count monitoring ^17,3. As a topical gel, the same molecule became a mild prescription acne treatment whose systemic absorption is roughly one percent of an oral dose ¹.

This site keeps the two lives separate on every surface. The same species-and-route-labeled study table that grades the acne gel's honestly modest trial numbers also grades the oral drug's seven decades of evidence, and the safety sections state which route each risk belongs to ²⁹. Dapsone is FDA-approved both as a topical acne gel (Aczone and generics) and as oral tablets for dermatitis herpetiformis and leprosy.

The fact chips below are each sourced: chemistry from PubChem and the FDA labels, exposure numbers from the label pharmacokinetics sections, risk numbers from the label warnings and the primary literature. The single most useful number on this page: oral exposure is about 100 times topical exposure for the same molecule ². Almost every honest safety statement about dapsone follows from it.

Dapsone is FDA-approved both as a topical acne gel (Aczone and generics) and as oral tablets for dermatitis herpetiformis and leprosy. That disclosure is unusual for this fleet: most compounds we cover are approved in one form and sold in another, or not approved at all. Dapsone is approved in both of its market forms. The honesty problem here is not a status gap; it is the borrowing of one route's story by the other.

The paper trail: ACZONE gel 5% was approved July 7, 2005 under NDA 021794 ⁴; ACZONE gel 7.5% followed on February 24, 2016 under NDA 207154 ⁵. Drugs@FDA lists 29 dapsone applications across both routes, including at least 7 marketed generic 5% gels, 7 generic 7.5% gels, and 8 oral tablet applications at 25 mg and 100 mg ⁶. Every one is prescription-only: dapsone has no over-the-counter form and is not an ingredient in FDA's OTC acne monograph (benzoyl peroxide, at 2.5 to 10 percent, is) ⁹.

One label even has a regulatory history worth reading: the original 2005 Aczone label required a G6PD level in all patients before starting. FDA deleted that requirement in the March 2008 revision after a dedicated crossover trial in G6PD-deficient patients, and today's gel labels require no blood testing at all ^7,8,1. The full story is in the G6PD section, because it is the cleanest documented example of a topical label shedding an oral-grade precaution once route-specific data existed ¹⁵.

Topical (gel, 5% and 7.5%): acne vulgaris. The 7.5% gel is indicated for patients 9 years of age and older; the 5% gel's trials enrolled ages 12 and up ^1,2. That is the entire approved topical indication: no rosacea, no eczema, no off-label promises on this site.

Oral (tablets, 25 mg and 100 mg): dermatitis herpetiformis, and all forms of leprosy except proven dapsone resistance. The label calls dapsone a primary treatment for dermatitis herpetiformis, and for leprosy it is used only in combination regimens: WHO multidrug therapy pairs it with rifampicin and clofazimine ^3,10.

Everything else dapsone is used for, from Pneumocystis prophylaxis in HIV medicine to a long list of neutrophilic dermatoses, is off-label practice, and this site grades that evidence where it exists rather than folding it into the approved list ^38,29.

Here is the number that separates dapsone's two lives. In the crossover pharmacokinetic study, two weeks of dapsone gel 5% applied twice daily to about 22.5% of body surface area produced a daily exposure (AUC) of 415 ng.h/mL. A single 100 mg oral tablet, in the same study, produced 52,641 ng.h/mL: roughly 100 times more drug in the blood from one pill than from a day of maximal gel use ^2,17.

The 7.5% gel sits even lower. At steady state its peak plasma concentration is 13.0 ng/mL and its daily AUC is 282 ng.h/mL, which the label rounds to about 1% of a 100 mg oral dose ¹. Patients on chronic oral dapsone for dermatitis herpetiformis, by contrast, carry plasma levels around 2,300 ng/mL, about 175 times the gel's peak ^36,1.

That two-orders-of-magnitude gap is why the same molecule behaves like two different drugs. At oral exposures, hemolysis is near-universal: the oral label states that almost all patients lose 1 to 2 g of hemoglobin, run reticulocytes up 2 to 12%, and carry elevated methemoglobin ³. At topical exposures, the pivotal trials could not tell dapsone's side-effect profile apart from the vehicle gel ¹.

Both directions of borrowing are wrong. Skincare marketing that dresses the acne gel in the oral drug's gravitas (a leprosy drug for your breakouts) is exaggerating a 1% exposure into a systemic therapy. Skincare reassurance that waves off dapsone's hematology entirely is forgetting that the gel's own postmarketing record includes hospitalization-level methemoglobinemia, including in a toddler who got into a sibling's pump ^1,35. The route divide is quantitative, not absolute.

For acne, the honest answer comes from the label itself: the mechanism of action of dapsone gel in treating acne vulgaris is not known ^1,2. Both gel labels carry that sentence verbatim. A 60-year-old drug, two approvals, and no settled mechanism for its acne effect: that is a real and instructive fact about dermatology, and we would rather quote it than invent a tidy story.

What is documented sits one level down. As an antimicrobial, dapsone is bactericidal and bacteriostatic against Mycobacterium leprae (the oral label's kinetic-method-in-mice statement), and resistance emerged historically when it was used alone, which is why leprosy treatment became combination therapy ^3,1. As an anti-inflammatory, the best-characterized action is in vitro: at concentrations matching therapeutic blood levels (1 to 30 mcg/mL), dapsone competitively inhibits the myeloperoxidase-H2O2-halide cytotoxic system in neutrophils without touching chemotaxis, ingestion, or lysosomal release ²⁷. Reviews add effects on adhesion molecules, IL-8 and TNF-alpha signaling, again mostly from in vitro work ²⁸.

Note what that means for the acne gel: the neutrophil-suppression story is a plausible transfer from the dermatitis herpetiformis literature, not a demonstrated acne mechanism, and the therapeutic concentrations in that in vitro work are oral-range levels the gel never reaches in plasma (skin concentrations are another matter and are not published). We label the mechanism rows accordingly ^27,29.

The gel, per its labels: wash and pat dry, then apply approximately a pea-sized amount in a thin layer. The 7.5% gel goes on once daily to the entire face, plus other affected areas; the 5% gel goes on twice daily to acne-affected areas. Both labels say the same thing about patience: if there is no improvement after 12 weeks, reassess ^1,2. Supplied sizes are 30, 60 and 90 gram pumps (7.5%) and tubes (5%) ^1,2. Our application-quantity tool does the arithmetic from these label quantities and the fingertip-unit standard (face and neck take about 2.5 FTU, roughly 1.25 g per application) and states which numbers are label text and which are the FTU convention ²³.

The oral tablets, per their label: dermatitis herpetiformis starts at 50 mg daily in adults, titrated between 50 and 300 mg to the minimum dose that controls symptoms; a strict gluten-free diet lets many patients taper off entirely, on a timescale of months to years ³. Leprosy regimens use 100 mg daily in combination with rifampicin (and clofazimine in WHO multidrug therapy), never as monotherapy ^3,10.

This page is education, not a prescribing reference: oral dapsone is specialist territory with mandatory blood-count monitoring, and the numbers above are quoted so you can recognize standard practice, not reproduce it ³.

The study table below carries every study and evidence source this site relies on, one row each, with species, route, design grade, size, dose, duration, outcome and effect size. Two things are unusual about dapsone's table. First, it is almost entirely human: this is a drug with pivotal programs in the thousands of patients, not a rodent-extrapolation compound; the exact row counts render as script-verified site statistics. Second, the route column does real work: topical acne evidence and oral systemic evidence sit in the same table but never blend.

The shape of the evidence, honestly summarized: the acne gel's efficacy is real and statistically solid across four randomized trials totaling over 7,300 patients, and modest in size, with vehicle-adjusted differences of about 7 to 10 percentage points on clear-or-minimal skin and 1.6 to 8 percentage points on lesion reductions ^12,13,14,2. The oral drug's dermatitis herpetiformis role rests on 70 years of consistent clinical experience and guideline consensus with zero efficacy RCTs ^43,24. The leprosy role is anchored by WHO multidrug therapy with about 4% pooled relapse ⁴⁰. Strong evidence is not all the same shape; the grades say which shape each claim has.

The 5% gel earned approval on two identically designed 12-week randomized vehicle-controlled trials totaling 3,010 patients ¹². On the label's own tables: 42% of dapsone patients versus 32% of vehicle patients reached no-or-minimal acne in study 1; 35% versus 28% in study 2. Inflammatory lesions fell 46% versus 42%, and 48% versus 40% ². Read those twice: the vehicle gel did most of what the drug gel did. The drug's edge is 7 to 10 points of responders, 4 to 8 points of lesion reduction.

The 7.5% gel's two trials (2,102 and 2,238 intent-to-treat patients) tell the same story once daily: treatment success 29.9% versus 21.2% and 29.8% versus 20.9%; inflammatory lesions down 55.5% versus 49.0% and 53.8% versus 47.3% ^13,14. On absolute counts, dapsone removed about 16 inflammatory lesions to vehicle's 14: a difference of roughly two pimples at week twelve ¹. All of these differences are statistically robust (P<.001) because the trials were huge; statistical certainty about a modest effect is still a modest effect.

Context from the rest of the field: a 2022 systematic review of 14 studies puts topical dapsone's success rates at 40.1 to 69.4% (5%) and 29.8 to 47.0% (7.5%), always stronger on inflammatory lesions ¹⁹. The 2024 AAD guideline's strong recommendations go to benzoyl peroxide, topical retinoids, topical antibiotics and doxycycline; its named conditional list covers clascoterone, salicylic acid and azelaic acid; topical dapsone appears in neither named list in the guideline abstract ²¹. And no head-to-head randomized trial against benzoyl peroxide or azelaic acid monotherapy exists; the one randomized combination study found that adding benzoyl peroxide or adapalene to dapsone gel did not significantly beat adding moisturizer (P=0.052) ^44,20.

What dapsone gel genuinely offers is tolerability and a niche: application-site dryness at 1.1% versus 1.0% on vehicle, pruritus 0.9% versus 0.5%, a 12-month open-label study with 8.2% application-site reactions and no hematology changes, and a formulation logic aimed at patients who cannot tolerate the stronger first-line topicals ^1,16. That is the honest sales pitch the trials support: gentle, real, modest ¹⁹.

Dermatitis herpetiformis (DH) is the gluten-driven blistering disease: intensely pruritic papules and vesicles with granular IgA deposition, sitting on the same immunology as celiac disease ²⁴. Dapsone's place in it is unlike anything else on this site: the oral label itself calls dapsone a primary treatment for the disease, and in responsive patients the label describes a prompt reduction in itch followed by clearing of lesions ³. Dermatology has used the response speed as a practical diagnostic hint for decades.

Now the honest part. No randomized controlled trial of dapsone's efficacy in DH has ever been run. PubMed's RCT filter over DH and dapsone returns exactly two small NSAID-interaction experiments, not an efficacy trial ^43,26. The evidence base is 1955 Lancet reports, seventy years of uncontrolled but remarkably consistent clinical experience, label recognition, and a 2021 European consensus guideline that is explicit about being expert-based (S2k level) ^25,24. We grade all of that exactly as what it is. It is strong evidence of the old kind: universal, durable, and untested by modern methods because nobody doubted it enough to randomize it.

Two more label facts complete the picture. Dapsone treats the skin, not the gut: it has no effect on the gastrointestinal component of the disease ³. And the exit ramp is dietary: on a strict gluten-free diet, the average patient can reduce the dose after 8 months and stop entirely after 29 months (ranges stretch to years) ³. Dapsone is the bridge; the diet is the treatment.

Dapsone was the first widely effective leprosy drug, and it is still there: WHO multidrug therapy (MDT) combines dapsone, rifampicin and clofazimine, supplied free of cost through WHO, with 6-month courses for paucibacillary and 12-month courses for multibacillary disease ^10,39. The US oral label tells the same story with its own institutions: 100 mg daily, always in combination, per the WHO Expert Committee and the US Public Health Service ³.

The combination exists because of dapsone's own history: therapeutic resistance in Mycobacterium leprae emerged under oral monotherapy, a fact both labels record ^1,3. Within MDT the results are good: a 2025 meta-analysis across 26 studies and 71,385 participants put pooled relapse at about 4% (95% CI 2 to 5%) with regular MDT ⁴⁰. Annual new case detection worldwide plateaued around 200,000 before the pandemic ³⁹.

Why this matters on an acne-adjacent site: the leprosy pedigree is exactly the kind of borrowed gravitas the route divide warns about. It certifies the molecule's systemic power at oral exposures; it says nothing about what a 1%-exposure gel does for pimples. We keep the rows separate so neither story inflates the other ².

Dapsone's third life was in HIV medicine. In the ACTG randomized trial of 843 patients with advanced HIV, dapsone prophylaxis held the 36-month risk of Pneumocystis pneumonia to 17%, statistically comparable to trimethoprim-sulfamethoxazole's 18% and better than aerosolized pentamidine's 33% in the sickest stratum; 100 mg outperformed 50 mg ³⁸. Modern guidelines keep dapsone as an alternative agent for patients who cannot take TMP-SMX; that use is off-label and belongs to infectious-disease practice, not consumer skincare.

In dermatology beyond DH, reviews catalog dapsone's use across neutrophilic disorders (linear IgA disease, and a range of others), where it has been most successful in conditions marked by abnormal neutrophil and eosinophil accumulation ²⁹. Nearly all of that literature is uncontrolled: case series and clinical experience, graded here as exactly that. We list it to map the molecule honestly, not to recommend it ²⁸.

The question needs a route attached. Is the acne gel safe? In 12-week trials of over 4,300 patients, its adverse-event profile was statistically indistinguishable from the vehicle gel, and a 12-month open-label study added no hematologic signals; its labels list literally no contraindications ^1,16. Is the oral tablet safe? It is a drug whose label opens its warnings with reported deaths from agranulocytosis and aplastic anemia and prescribes a blood-count calendar ³. Same molecule, different answer, because the dose differs by two orders of magnitude ².

The gel's serious risks are real but rare, and they are the oral risks leaking through at case-report frequency: methemoglobinemia with hospitalization has been reported postmarketing, and G6PD-deficient users can show mild laboratory hemolysis ¹. The oral drug's risks are common and expected: near-universal dose-related hemolysis, 1.4% hypersensitivity syndrome with about 10% fatality when it strikes, and roughly 1-in-3,000-patient-years agranulocytosis ^3,31,30.

One reassurance holds across routes: dapsone is a sulfone, not a sulfonamide antibiotic, and cross-reaction with sulfa allergy has not been demonstrated ⁴². The sections below take each risk in turn, as questions.

Three blood problems define oral dapsone, in descending frequency. Hemolysis: dose-related, near-universal (a 1 to 2 g hemoglobin loss with reticulocytosis in almost all patients), worse with G6PD deficiency ³. Methemoglobinemia: dapsone is the single most common drug cause in hospital series, responsible for 42% of 138 cases in the two-hospital Medicine series, with mean peak levels of 7.6% ³³. Agranulocytosis: rare but lethal when missed, about 1 case per 3,000 patient-years in the Swedish DH registry (1 per 240 to 425 treated patients), typically in the first months; the label's response is the CBC calendar and an instruction to react to sore throat, fever, pallor, purpura or jaundice ^30,3. Deaths from agranulocytosis and aplastic anemia are on the label's first warning line ³.

The topical translation of each: hemolysis shrinks to transient laboratory changes in G6PD-deficient users (next section); agranulocytosis has not been observed in gel trials; methemoglobinemia survives as the gel's one hospital-grade postmarketing risk, with published cases including a toddler exposed to a sibling's gel and an NEJM adult case, and the labels instruct anyone with slate grey cyanosis of lips, nail beds or mouth to stop and seek immediate care ^1,35,34.

The antidote chapter belongs to this site's sister compound: for serious dapsone methemoglobinemia the oral label names intravenous methylene blue, 1 to 2 mg/kg, as the treatment of choice, repeatable on rebound, and unusable in fully expressed G6PD deficiency where the reduction pathway it needs does not work ³. Peripheral neuropathy and severe skin reactions round out the oral list; neither was observed in the topical trials ¹.

Dapsone hypersensitivity syndrome (DHS) is the drug's version of DRESS: fever, rash, organ involvement (notably hepatitis), typically weeks into oral therapy. The systematic review across 336 reported patients puts its prevalence at 1.4% of treated patients (95% CI 1.2 to 1.7%) and its fatality rate at 9.9%; mucosal involvement, hepatitis, older age and treatment in non-affluent countries predicted death ³¹. The NEJM genetics paper frames the background incidence as 0.5 to 3.6% of treated persons ³².

The genetics are among the cleanest in pharmacogenomics: HLA-B*13:01 carries an odds ratio of 20.53 for DHS in leprosy patients, predicting the syndrome with 85.5% sensitivity and 85.7% specificity; absence of the allele cuts risk from 1.4% to 0.2%. The allele is common in parts of Asia (2 to 20% of Chinese, 1 to 12% of Indians) and largely absent in Europeans ³². Screening programs exist in leprosy medicine; nothing analogous is established for dermatology, and the study population was leprosy patients, a limit we flag rather than smooth over ³².

For the gel: DHS is an oral-exposure phenomenon in the published record, and skin reactions of the severe class were not observed in topical trials; the gel labels still carry the oral experience as class information ¹.

By route, per the actual labels. Oral: the label handles G6PD deficiency as a live clinical issue: hemolysis and Heinz-body formation may be exaggerated, the reaction is dose-related, give with caution, treat severe anemia first, monitor hemoglobin ³. In practice that is why G6PD status is established around oral dapsone therapy. Topical: neither current gel label requires any G6PD testing. The warnings note that G6PD-deficient users may be more prone to methemoglobinemia and hemolysis and that some developed laboratory changes suggestive of hemolysis, and section 8.6 reports the dedicated trial ¹.

It was not always so, and the change is the interesting part. The original July 2005 Aczone label required G6PD levels in all patients prior to starting. Then came the purpose-built study: a randomized, double-blind crossover of 64 G6PD-deficient acne patients, which found a 0.32 g/dL hemoglobin dip at two weeks that vanished by week twelve on continued treatment, 1-g/dL drops as common on vehicle as on drug (7 of 56 versus 8 of 58), the single largest drop in the vehicle group (1.7 versus 1.5 g/dL), and no clinical hemolytic anemia ^15,2. FDA deleted the screening requirement in the March 2008 label revision ^7,8. A label walking back a precaution because route-specific data arrived is regulatory honesty working as designed, and it is the strongest single piece of evidence that the gel's hematology genuinely differs from the tablet's.

Scale matters here: G6PD deficiency is the most common human enzyme deficiency, an estimated 400 million people, concentrated in populations of African, South Asian, Middle Eastern and Mediterranean ancestry ^41,1. The practical gel-era cautions that remain: do not combine the gel with oral dapsone or antimalarials, and know that trimethoprim/sulfamethoxazole raises dapsone levels and hemolysis risk in G6PD deficiency ¹. Our G6PD tool walks each label's language by route.

Gel: the trial numbers are almost comically vehicle-like. Application-site dryness 1.1% versus 1.0% on vehicle; pruritus 0.9% versus 0.5%; overall adverse events 19.1% versus 20.6% and 17.6% versus 17.1% across the two 7.5% trials ^1,13,14. The 5% program's four vehicle-controlled trials showed the same mirror-image pattern, and the 12-month study logged 8.2% treatment-related application-site reactions with no hematology or chemistry changes ^2,16. Postmarketing adds the serious rarities: methemoglobinemia, rash, and facial swelling ¹.

Oral: expected effects at treatment doses include the hemolysis package (1 to 2 g hemoglobin loss, reticulocytosis, methemoglobin rise) in almost all patients ³. The label's longer list runs from nausea and headache through photosensitivity to rare organ-level events, and its serious tier (agranulocytosis, hypersensitivity syndrome, neuropathy, severe skin reactions, hepatitis) is covered in the sections above ³.

Gel, pregnancy: there are no human data. The label's reasoning is exposure-based: topical absorption is low relative to oral dosing, and the animal signal (embryocidal effects in rats and rabbits) appeared only at oral exposures more than 400 times the maximal topical human exposure, probably secondary to maternal toxicity ¹. No-data is the honest headline; the exposure math is the context.

Oral, pregnancy: Category C under the older system. Extensive but uncontrolled experience and two published surveys have not shown increased fetal abnormalities; the label notes dapsone has been important for managing some pregnant DH patients, and leprosy authorities recommend maintaining therapy ³. That is decades of reassuring but uncontrolled human experience, not trial evidence.

Breastfeeding differs by route in the label's own words: oral dapsone is excreted in breast milk in substantial amounts and hemolytic reactions can occur in neonates, especially G6PD-deficient infants; for the gel there is no direct milk data, and its label falls back on the low-absorption argument while telling patients not to combine breastfeeding with use without a decision ^3,1. Decisions here belong with the prescriber; this page's job is to show which facts exist for each route.

The interaction everyone using the gel should know is cosmetic and startling: benzoyl peroxide applied with topical dapsone can temporarily stain skin and facial hair yellow or orange at the site. It is on the label twice, in the interactions section and the patient leaflet ¹. Since benzoyl peroxide is the default acne active, this is the single most likely dapsone interaction in real life. It is temporary and local; the fix is separating the two in time per your prescriber's instructions.

Systemic interactions scale with route. Trimethoprim/sulfamethoxazole raises dapsone and metabolite levels (the gel label notes gel exposure stays around 1% of oral even then; the oral label quantifies the trimethoprim interaction at about 1.5 times each way) ^1,3. Rifampin drops oral dapsone levels 7 to 10-fold. Folate antagonists like pyrimethamine raise hematologic risk. Methemoglobinemia-inducing drugs (benzocaine, nitrates, primaquine, sulfonamides and a label-listed crowd of others) stack with dapsone's own methemoglobin effect ^3,1.

One interaction is actually therapeutic and shows the metabolism plainly: cimetidine blocks formation of the hydroxylamine metabolite that drives methemoglobinemia, and in small human studies cut methemoglobin from 5.5% to 3.9% while dapsone levels rose about 30% and disease control held ^36,37. And the gel carries its own avoid-list: no concurrent oral dapsone, no antimalarials ¹.

The oral label's schedule, quoted because it is the clearest expression of the route divide: complete blood counts weekly for the first month, monthly for six months, and semi-annually thereafter, per the FDA Dermatology Advisory Committee; discontinue if leucocytes, platelets or hemopoiesis drop significantly ³. Add baseline and periodic liver function when feasible (toxic hepatitis and cholestatic jaundice occur early in therapy), severe-anemia correction before starting, and hemoglobin monitoring in G6PD-deficient patients ³.

The topical monitoring requirement, for contrast, is: none. No CBCs, no G6PD level, no laboratory schedule appears in either current gel label; the labels instead teach symptom recognition (cyanosis, signs of hemolysis) ^1,8. When a skincare article tells acne patients they need blood work for dapsone gel, it is quoting the wrong route; when a wellness article calls oral dapsone monitoring optional, it is contradicting the label's first warning ³.

Topical, 7.5% once daily at steady state (2 g/day coverage): Cmax 13.0 ng/mL, AUC(0-24) 282 ng.h/mL, steady state within 7 days, about 1% of a 100 mg oral dose ¹. Topical, 5% twice daily (14 days, 22.5% BSA): AUC 415 ng.h/mL against 52,641 ng.h/mL for a single oral 100 mg dose in the same crossover: the 100x line every other number on this page orbits ^2,17. Curiously, the stronger gel delivers less drug systemically: the 7.5% once-daily formulations ran 25 to 40% below the 5% twice-daily gel in daily exposure ¹⁸.

Oral: peak at 4 to 8 hours; half-life 10 to 50 hours averaging 28; steady-state levels around 2.3 mcg/mL at 200 mg daily (patients on chronic 50 to 100 mg run around 2.3 mcg/mL troughs in the cimetidine studies); about 85% of the dose is recoverable in urine as water-soluble metabolites ^3,36. Acetylation rate variation matters clinically (the label flags fast acetylators for dose adjustment), and the hydroxylamine metabolite, not the parent, drives the methemoglobin toxicity, which is exactly why cimetidine's pathway block helps ^3,37.

Both gel presentations store at controlled room temperature, 20 to 25 C (68 to 77 F), with excursions permitted to 15 to 30 C; protect from freezing. The 7.5% ships as 30, 60 and 90 gram airless pumps; the 5% as 30, 60 and 90 gram laminate tubes ^1,2. Oral tablets store at the same range, protected from light, in child-resistant bottles; the toddler methemoglobinemia case is the standing argument for keeping every dapsone product away from children ^3,35.

Answers below are the 320-character direct answers our machine layer serves, expanded with citations. Every answer states which route it is about, because almost no dapsone question has a route-free answer.

Every citation below was fetched and verified during pack construction with the source archived. Journal links point to Europe PMC abstract pages (with PubMed alternates); label links point to DailyMed; regulatory links to accessdata.fda.gov and eCFR. The machine-readable citation manifest this page ships mirrors this list one-to-one.