An incidence-to-eligible funnel built as a live, re-runnable Excel model: 8 sheets, 119 formulas, zero hardcoded cells. Every conversion step sourced, every assumption editable.
Incidence-to-eligible NSCLC funnel by cohort with sourced conversion assumptions and a share waterfall.
100,000-200,000 US gMG patients narrow to a 4,000-6,000 on-FcRn-therapy pool, and 1,200-2,100 of them remain inadequately controlled despite treatment.
12,000-15,000 UK gMG patients on the broader estimate, of whom ~4,000 have moderate-severe disease and 2,000-3,000 are refractory, with no NICE-recommended novel agent for any of them.
An estimated 100,000 US sickle cell disease patients narrow to a 55,000-65,000-patient pool with no adequate novel therapy, while only 50-100 of the gene-therapy-eligible minority were actually treated in year one.
5,000-10,000 diagnosed US classic Fabry patients, a 35-50% amenable-mutation gate to oral therapy, and a treated population still 60-65% on enzyme replacement. This funnel starts at diagnosis because no defensible undiagnosed estimate exists yet.
6,000-10,000 GCC gMG patients on the epidemiology estimate, of whom 200-300 are refractory and fewer than 50 are currently on biologic therapy.
15,000-17,000 diagnosed UK sickle cell disease patients, universal since 1999 newborn screening, narrow to a 4,000-6,000-patient conventional-therapy gap and a separate 200-300-per-year gene-therapy-eligible pool.
700-900 NHS-diagnosed Fabry patients split cleanly: roughly 600 on enzyme replacement, about 200 (25%) on oral migalastat, and free NHS cascade testing that adds 3-4 diagnosed relatives per index case.
6,000-8,000 US Dravet patients, roughly three-quarters SCN1A-confirmed, and 35-40% still inadequately controlled on cannabidiol plus fenfluramine, the population any new agent must actually reach.
8,000-10,000 US SMA patients, a Type 1-4 severity split running roughly 60/27/13/under 5 percent, and the 500-700-patient Zolgensma cohort this funnel validates against.
GCC male Fabry prevalence runs 1:20,000-30,000, elevated by founder mutations, yet only 200-300 patients are diagnosed against a true burden estimated 3-5 times higher, and female diagnosis lags under half the male rate.
500,000+ US patients aged 70+ with HFpEF carry undiagnosed ATTRwt-CM, against only 70,000-100,000 diagnosed and treated. Two further sub-populations, Val122Ile carriers and ATTR-PN, remain even less visible.
2,000-2,500 UK Dravet patients, of whom 400-500 are SCN1A-molecularly-confirmed in genetic registries, and 600-900 still inadequately controlled on cannabidiol plus fenfluramine.
An estimated 8,000-9,000 Americans live with hereditary angioedema. Just 35-40% receive any prophylaxis, leaving 2,500-4,000 patients who meet treatment criteria untreated, the funnel this model sizes precisely.
True UK ATTRwt-CM prevalence runs 20,000-40,000, and 15,000-36,000 of those patients remain undiagnosed. Only 3,000-4,000 are on NHS-commissioned tafamidis today, adding 1,500-2,000 a year.
A ~1,000-patient confirmed UK SMA cohort by type, reconciled against a 1,800-2,000-patient total prevalence estimate, and a 50-60/yr Zolgensma cohort as the on-therapy validation anchor.
600-800 estimated GCC Dravet patients, fewer than 200 SCN1A-molecularly-confirmed, and a 200-400 near-term addressable cohort within that confirmed subset.
The UK HAE Alliance counts 5,000-6,000 total patients, of whom 1,500-2,000 are on NICE-commissioned prophylaxis. A further 1,500-2,500 are attack-active but never treated, and Longhurst et al.'s 37-centre registry confirms 1,152 patients from the bottom up.
15,000-20,000 Americans carry a PNH clone, but only about 3,500 reach complement-inhibitor therapy, and up to 1,200 of them stay anemic on it. This model sizes every gap in between.
GCC SMA incidence of 1:6,000-8,000 births, country-level newborn-screening coverage from 90% down to under 50%, an 800-1,200-patient legacy Type 2/3 pool, and a 60-80/yr Zolgensma cohort as the on-therapy anchor.
Epidemiology projects 1,200-1,500 GCC HAE patients; the GCC allergy society's own case registry counts only 400-600. The gap is not a contradiction, it is the diagnostic-capacity constraint of just 6-10 specialist physicians across all six states.
Two GCC ATTR-CM burden estimates, 15,000-25,000 and a narrower 2,000-5,000 ATTRwt-CM cohort, both convert to fewer than 1,000 confirmed diagnoses. This model reconciles the gap and traces it to scintigraphy access.
~600-750 UK PNH patients are on active complement-inhibitor therapy against a reconciled total prevalence near 1,500; the other 750-900 are monitored-only or undiagnosed, and this model sizes the gap.
5,000-10,000 Americans live with Pompe disease. Roughly 2,000 late-onset patients are on enzyme replacement therapy, and 375-600 of them, one in four, are inadequate responders, the subtype this model is built to size.
France's PMSI hospital database counts 897 PNH patients over five years; Orphanet's older estimate puts national prevalence at 850-1,000. Only 270 of them, per the manufacturer's own estimate, are eligible for a second-line oral agent.
350-450 UK Pompe disease patients, of whom roughly 200 form the registry-confirmed cohort. One in four long-term ERT patients is not holding stable, the segment this model is built to size.
400-600 GCC Pompe disease patients, of whom 200-300 are on enzyme replacement therapy. Just 40-60, patients with FVC decline despite alglucosidase already on home ventilation, are the segment this model is built to size.
200,000-250,000 GCC-wide sickle cell disease patients (140,000-200,000 in Saudi Arabia alone), but NPHC's actively-managed registry reaches only 8,000-10,000 — the addressable near-term funnel stage within a much larger under-managed population, not a contradiction.
An estimated 2,000-3,000 Gulf patients carry a clinically significant PNH clone, but only about 400 are confirmed in national registries, and just 150-250 reach complement-inhibitor therapy. Diagnostic capacity, not drug access, is the constraint this model sizes.
Germany has no domestic PNH prevalence count of its own; DGHO's Onkopedia guideline borrows a 16-per-million estimate from British and French registries. Only two national centres, Ulm and Essen, anchor referral.
An estimated 8,000-12,000 GCC IgAN patients narrow to fewer than 30% ever biopsied, then to zero on novel therapy, since no agent is SFDA-registered as of 2024. The funnel gap, not the prevalence estimate, is what a GCC patient flow model has to size.
150,000 US IgA nephropathy patients, of whom 70,000-90,000 are biopsy-confirmed. Only 5,000-8,000 are on novel therapy today, while 15,000-25,000 patients with UPCR above 1g/g remain the addressable high-risk cohort this model sizes precisely.
10,000-15,000 UK IgA nephropathy patients, of whom approximately 8,000 are tracked in the UK Renal Registry. Only 3,000-5,000 clear the mandatory ACEi/ARB and SGLT2i optimisation gate to become eligible for a novel agent, and fewer than 500 currently access one pre-NICE.
316,950 new US invasive breast cancer diagnoses in 2025. Only 6.0% present as metastatic at diagnosis, but 73.9% of the metastatic population is HR+/HER2-, the subtype this model is actually built to size.
An editable Excel funnel model, a PDF write-up of the assumptions and result, and a PowerPoint readout, with a 45-minute analyst call included.
Every conversion is cited to a primary source and re-runnable; the model shows its working rather than a black-box number.
Yes. You set the market, cohort definition and comparators; the model is built to your scope and delivered editable.