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Longevity: The Science and Business of Aging

The biology of aging, what can slow it, who is funding the cure, and why there is still no approved drug.

Aging is the largest shared risk factor for death, disease and cost on Earth, and a century of animal data says it can be slowed. Yet not one drug is approved to treat it. The gap between what the biology allows and what the market has delivered is the entire investment story.

Chapters
10
Reading time
31 min
Updated
110,000Deaths a dayfrom age-related disease worldwide
x2 / 8 yrsMortality doublingrisk of death after age 30 (Gompertz)
$1-2BAging R&D / yearjust 0.25-0.5% of biomedical spend
0Drugs approvedfor aging as an indication, anywhere

What this argues

  1. Aging drives the disease burdenIt drives the fiscal burden too: trillions, unnamed.
  2. Slowing it is proven in animalsCalorie restriction and rapamycin, repeatedly.
  3. Humans remain unprovenHype has outrun human evidence for decades.
  4. Regulation is the real barrierAging is not yet an approvable indication.
  5. Watch the endpoints, not the micePROSPR, Loyal, and the first human wins.
00

What has changed

Updated November 2026

$144MARPA-H PROSPR ceilingseven teams, five years (Feb 2026)
$435MNewLimit Series CJune 2026
$100MLoyal Series CFeb 2026, led by age1; $250M+ raised in total
0Drugs approved for aginghuman or canine, as of the sources read
February 2026

ARPA-H funded seven PROSPR teams

  • Up to $144M over five years, structured as milestone-based contracts rather than grants (Longevity.Technology, 25 Feb 2026).
  • Teams include Cambrian BioPharma (up to $30.8M, an oral rapamycin analog), Linnaeus Therapeutics (up to $22M), and a UT Health San Antonio phase 3 hybrid trial of an SGLT2 inhibitor, rapamycin and semaglutide.
  • Stanford and Columbia work on biomarkers, harmonized data and endpoints; the aim is early surrogate endpoints that show an aging shift within one to three years.
January and February 2026

Loyal raised $100M and cleared the safety step

Loyal announced a $100M Series C led by age1 on 11 Feb 2026 (Loyal press release), bringing total capital to over $250M. Its LOY-002 dog pill has had the effectiveness and target animal safety sections accepted by FDA CVM for Expanded Conditional Approval (safety accepted January 2026); the third requirement was in progress and Loyal planned to submit it later in 2026. The 1,300-dog STAY study had completed enrollment and has no final results yet (Fortune, 11 Apr 2026). No approval was found as of the sources read.

June 2026

First patient dosed in a human reprogramming trial

Life Biosciences announced on 9 Jun 2026 that the first participant was dosed in a Phase 1 trial of ER-100 (OSK partial reprogramming) for open-angle glaucoma and NAION, registered as NCT07290244. The trial primarily tests safety and tolerability, with visual function as additional endpoints (Life Biosciences release).

April to June 2026

Large private rounds continued

  • NewLimit: $435M Series C, 2 Jun 2026, to take its first epigenetic reprogramming medicine toward human trials (Cure longevity funding tracker, Jul 2026).
  • Retro Biosciences: initial close of a new round at a $1.8B pre-money valuation, 22 May 2026 (same tracker); amount undisclosed.
  • Life Biosciences: $80M Series D, 8 Apr 2026 (same tracker).

Not refreshed: capital-raised chart totals for Calico, Altos, NewLimit, eGenesis and Life Biosciences (cumulative figures could not be reconciled with the new rounds); Altos Labs 2026 funding (nothing found); TriviumVet cat approval status; organ-transplant counts; pharma pipeline percentages; demographic and GDP figures; the 30-year trial estimate.

Test yourself

A headline says a human reprogramming trial has started. What does the Life Biosciences ER-100 trial primarily test?

What is the main aim of the Stanford and Columbia work inside the ARPA-H PROSPR program?

00

Orientation

How to read this deck

Orientation

How to read this deck

  • Aging is one process. We treat it as a single risk factor, not a list of diseases.
  • Separate proof from hype. We flag what is shown in mice, in humans, and merely claimed.
  • Follow the money and the rules. The bottleneck is regulatory and financial, not biological.
  • Every figure is dated. Sourced to primary studies; estimates are marked as such.

Test yourself

A supplement ad claims to reverse aging. Following the deck's approach, what should you do first?

According to the orientation, where does the main bottleneck for longevity medicine lie?

01

The Master Risk Factor

Why aging matters

Aging is the largest shared risk factor for death, disease and cost on Earth, and a century of animal data says it can be slowed. Yet not one drug is approved to treat it. The gap between what the biology allows and what the market has delivered is the entire investment story.

Executive summary

Longevity, in four numbers

110,000Deaths a dayfrom age-related disease worldwide
x2 / 8 yrsMortality doublingrisk of death after age 30 (Gompertz)
$1-2BAging R&D / yearjust 0.25-0.5% of biomedical spend
0Drugs approvedfor aging as an indication, anywhere

The single biggest risk factor for a heart attack is not smoking, blood pressure or cholesterol. It is age. A healthy 75-year-old is likelier to have a heart attack than a 20-year-old smoker with high blood pressure, high cholesterol and diabetes. Age is the master variable.

The shape of mortality

After 30, your risk of dying doubles every eight years

A line chart on a log scale plots annual risk of death (%) against age, from 25 to 100. The line climbs steadily across the whole range, rising by roughly two orders of magnitude between age 25 and age 100. Source: Gompertz-Makeham law of mortality.

How aging shows up

One driver, many failures

Ways aging shows up

FailureHow it shows up
Cardiovascularheart attack and stroke; age is the No. 1 risk factor.
Cancerincidence climbs steeply with every decade of life.
Dementianeurodegeneration rises sharply after 65.
EnduranceVO2 max falls; elite runners at 20 struggle on stairs at 70.
Strengthmuscle and grip decline, often before any visible loss.
Cognition & fertilityprocessing speed, memory and fertility all fall with age.
The geroscience payoff

Slowing aging beats curing any single disease

Added life-years (illustrative) yrs
View the data
Added life-years
Cure all cancers3
Cure heart disease4
Cure both + diabetes7
Slow aging10

Source: Science; The Milbank Quarterly (illustrative)

The demographic tide

Why this is a fiscal problem, not just a medical one

8.5% -> 16.7%Share aged 65+world, 2015 to 2050 (roughly doubling)
~$3T / yrUS outlay on 65+social + medical care, by 2029
+$400BUS GDP per yearfor each single year aging is slowed
+$2TUS GDPif aging slowed 5 years, over 2x defense

Test yourself

Someone's annual death risk at age 30 is 0.2%. If risk doubles every 8 years, roughly what is it at 46?

Why does the chapter say slowing aging could add more life-years than curing cancer or heart disease?

02

What Aging Is

The biology, honestly

There are almost as many theories of aging as there are researchers, but nearly all agree the genome sets the range, and damage fills it in. From a 58-day worm to a ~392-year shark, the same molecular parts yield wildly different lifespans. What divides the theories is whether aging is a program to switch off or damage to clean up.

Lifespan is written first in the genome

The same biochemistry, a ~2,500-fold range in lifespan

Lifespan, from days to centuries

SpeciesLifespan
Worm~58 days
Mouse~4 years
Human~122 years
Bowhead whale~211 years
Greenland shark~392 years
The central fork

Is aging something the body does, or something that happens to it?

Two families of theory

Program-based theoriesDamage-based theories
Claimaging is a genetic program still runningaging is passive wear and byproducts
Evidencesalmon 'suicide', ant queens, single-gene wormsDNA mutations, protein tangles, stiff matrix
The fixswitch the program offclean and prevent the damage
Weak spotthe examples may not generalize to humansdamage may be too diverse to ever fully repair
The damage, catalogued

Four ways bodies wear out

Types of damage

DamageWhat it is
DNA mutationstypos in the code that accumulate as cells divide; a driver of cancer.
Protein aggregationmisfolded proteins clump, the signature of Alzheimer's and Parkinson's.
Matrix crosslinkingsugars stiffen collagen and elastin: rigid arteries, aged skin.
Epigenetic driftthe tags that tell a cell what to be drift out of place over time.
The field's shared map

The Hallmarks of Aging, in three layers

Hallmarks of aging

LayerWhat it covers
Integrative hallmarksthe visible failures: stem-cell exhaustion, altered signaling, chronic inflammation, dysbiosis.
Antagonistic hallmarksprotective responses gone bad: cellular senescence, deregulated nutrient-sensing, mitochondrial dysfunction.
Primary hallmarksthe root damage: genomic instability, telomere attrition, epigenetic drift, lost proteostasis, disabled autophagy.

Test yourself

Which kind of damage does the chapter say reprogramming could in principle reset?

A worm lives about 58 days and a Greenland shark about 392 years, using the same basic biochemistry. What does this suggest?

03

Proof It Can Be Slowed

The animal evidence

Nature got there first

Species whose death risk barely rises with age

Negligibly senescent species

SpeciesNotes
Naked mole-rat30+ years; death risk does not rise with age, and cancer is rare.
Blanding's turtle~77 years; older females can reproduce better, not worse.
Rougheye rockfish200+ years; little sign of reproductive decline.
Red sea urchin100+ years (estimates run to 200); a textbook case of negligible senescence.
Greenland shark~392 years (est.); among Earth's longest-lived vertebrates.
Bowhead whale~211 years (est.); resists the cancers that should scale with its size.
The lab record

Every bar is a mouse that lived materially longer

Mouse lifespan extension %
View the data
Lifespan extension
Ames dwarf + CR75
Calorie restriction50
Ames dwarf (1 gene)50
Rapamycin + trametinib30
Rapamycin20
Young-donor stem cells12
Partial reprogramming9

Source: Various studies

A slow century, not a sudden breakthrough

The evidence base, stage by stage

  1. Gompertz's law: mortality found to double roughly every 8 years.
  2. Calorie restriction: underfed rodents live 30-50% longer, the first reliable lever.
  3. Yamanaka factors: adult cells can be reset toward youth; the seed of reprogramming.
  4. Rapamycin (NIH ITP): extends mouse lifespan even when started late.
  5. Drug combinations: rapamycin + trametinib add ~30% to mouse lifespan.
+10-25%Rapamycin's lifespan boost in micethe most replicated result in the field

It works even when started late in life, by damping mTOR, the cell's nutrient-and-growth sensor, so cells shift from growth toward repair. Yet it has never run a large human aging trial: it is off-patent, so no company will fund one.

Test yourself

What does 'negligibly senescent' mean for a species like the naked mole-rat?

Why has rapamycin never had a large human aging trial, despite strong mouse results?

04

Hype vs Evidence

The honest chapter

The credibility filter

Why most 'miracles' don't survive contact with rigor

  • The gold standard. NIH's Interventions Testing Program retests claims across three independent labs.
  • Most claims fail. Resveratrol, fish oil, curcumin and nicotinamide riboside showed no mouse lifespan benefit.
  • Rapamycin passed. One of the very few compounds to replicate, repeatedly.
  • Combinations can stack. Rapamycin + trametinib beat either drug alone (~30%).

No drug has ever been approved, anywhere, to treat aging, not because the science says it can't be done, but because the trial to prove it is nearly impossible to run. Aging isn't a recognized disease, all-cause-mortality trials take decades, and by the time one finished the patent would be long gone.

~30 yearsTo prove a single anti-aging drug works in healthy adults

A trial of 3,000 40-year-olds testing a drug that cuts death risk 20% would need roughly three decades and $300-350M to reach statistical significance, long after the patent expires. That math, not a lack of will, is why the trials don't happen.

What actually lowers mortality

Real, proven drugs, but for disease, not aging

All-cause mortality reduction %
View the data
Reduction in all-cause mortality
Statins14
SGLT2 inhibitors13
GLP-1 agonists12

Source: Cochrane Library; trial data

Do they touch aging, or one disease?

The test: acting on many diseases at once

DrugAll-cause mortalityActs beyond one disease?
Statins~14% lowerNo: the benefit is all cardiovascular
SGLT2 inhibitors~11-14% lowerPartly: heart, kidney and diabetes
GLP-1 agonists~12% lowerEmerging: heart, weight, a dementia signal
MetforminNo proven benefitNo: the aging case collapsed on review
The metformin lesson

How easily hope outruns the data

The 2014 claimThe 2022 correction
Finding: diabetics on metformin outlived non-diabeticsFlaw: the study quietly excluded sicker patients
Reaction: became the icon of anti-aging pharmaRedo: corrected, the survival edge vanished
Follow-on: inspired the TAME aging-trial effortMouse test: NIH's ITP found no lifespan benefit (2016)
Appeal: cheap, safe, ubiquitousLesson: extraordinary claims need replication
The honest ledger

Promising, but not yet proven in humans

Claims not yet proven

ClaimStatus
Senolyticsclear damaged 'zombie' cells; Unity's UBX0101 failed in knee osteoarthritis; none proven in humans.
Rapamycin in humansstrong in mice; off-patent, so untested at scale; proprietary analogs failed in the elderly.
Peptides & supplementsBPC-157, epitalon, NMN, methylene blue: little or no rigorous human data.
Blue zonesthe famous 'longevity hotspots': recent audits question the underlying records.

Test yourself

A trial of 3,000 40-year-olds tests a drug that cuts death risk 20%. Why is such a trial rarely run?

What went wrong with the 2014 metformin finding that diabetics outlived non-diabetics?

05

Four Strategies

The map of the field

One map for the whole field

Every longevity bet sits in one of four boxes

A two-by-two map. The horizontal axis runs from 'Buys time' to 'Stops & reverses aging'; the vertical axis runs from 'No deep theory' to 'Requires understanding aging'. Traditional Pharma and Advanced Bioengineering sit in the 'requires understanding aging' half (Traditional Pharma toward 'buys time', Advanced Bioengineering toward 'stops & reverses'); Biostasis and Replacement sit in the 'no deep theory' half (Biostasis toward 'buys time', Replacement toward 'stops & reverses').

The four strategies

Each strategy is a different bet on what aging is

StrategyThe bet
Traditional Pharmamodulate existing biology one target at a time; the default, best-funded path.
Advanced Bioengineeringadd new capabilities: partial reprogramming, gene and cell editing.
Replacementswap out aged parts: organs, tissues, ultimately (in theory) the whole body.
Biostasispause biology with extreme cold until better medicine exists.
Strategy 1: Traditional Pharma

The default path, and its cleverest workaround

  • Reuses the machinery. Leans on today's drug, regulatory and commercial infrastructure.
  • Back-door drugs. Rapamycin, SGLT2 inhibitors, GLP-1s: approved for disease, studied for aging.
  • Loyal (dogs). STAY trial in 1,300 senior dogs, enrollment complete: the first FDA-recognized aging study. Safety and effectiveness sections accepted; manufacturing section still pending (Feb 2026).
  • TriviumVet (cats). Extended-release rapamycin won FDA conditional approval, 2025.
Strategy 2: Advanced Bioengineering

The partial-reprogramming pathway

  1. Yamanaka factors (2006): four proteins reset an adult cell toward a stem-like state; Nobel 2012.
  2. Full to partial: brief exposure rejuvenates molecular markers without erasing cell identity.
  3. Animal results: muscle and nerve regeneration, less scarring, ~7-12% longer life in normal mice.
  4. First human trial (2026): Life Biosciences dosed its first patient in June 2026 (ER-100, glaucoma and NAION), not whole-body aging.
Reprogramming: promise and limits

Exciting and over-funded at the same time

What it can doWhat it can't
Rejuvenate. Resets epigenetic drift toward a younger stateDNA mutations. Survive reprogramming untouched
Regenerate. Optic nerve, muscle, less scarring in animalsMatrix crosslinks. Stiff collagen is unaffected
Extend life. ~7-12% in normal mice (two studies)Cancer risk. A full reset can turn cells tumorigenic
Reach humans. First FDA-cleared trial dosed its first patient in June 2026Close the gap. Billions raised; human evidence still thin
Strategy 3: Replacement

The ceiling is supply, not science

US organ supply versus need thousand
View the data
Count (thousands)
Waitlist adds (US, 2025)81
Transplants (US, 2025)49
End-stage deaths (2011)730

Source: OPTN; organ-preservation literature

Strategy 4: Biostasis

Stopping the clock

  • The idea. Cool the body until molecular decay effectively stops.
  • Proof it scales down. A rat kidney frozen to -150C, stored 100 days, was transplanted and worked (2023).
  • Nature's precedent. Wood frogs freeze solid; 46,000-year-old worms revived from permafrost.
  • The reality. 500+ people are already preserved; whole-body recovery remains unproven.

Test yourself

A startup grows gene-edited pig organs to swap into patients. Which strategy is this, and does it need a deep theory of aging?

Which statement about partial reprogramming is true, according to the chapter?

06

The Money

Where capital is flowing

A concentrated field

A handful of platforms hold most of the money

Capital raised by longevity platforms $M
View the data
Capital raised
Calico3500
Altos Labs3000
NewLimit755
eGenesis481
Life Biosciences250
Loyal250
Retro Biosciences180

Source: Company disclosures

The marquee bets

Who is building, and on what

CompanyRaised and focus
Altos Labs$3B; reprogramming; Bezos and Yuri Milner, the field's moonshot.
Calico$3.5B; Alphabet's secretive aging lab, running since 2013.
Retro Biosciences$180M (+$1B rumored; initial close of a new round at a $1.8B pre-money valuation, May 2026); Sam Altman-backed; reprogramming + pharma.
NewLimit$755M; Brian Armstrong; reprogramming, machine-learning-driven.
Life Biosciences$250M (before an $80M Series D in Apr 2026); first FDA-cleared reprogramming trial, first patient dosed June 2026 (the eye).
Unity Biotechnologysenolytics pioneer; its lead drug failed, a public cautionary tale.
Big pharma is circling, not committing

Most incumbents have no aging team, yet a third of their pipeline already targets aging

CompanyDedicated aging group?% pipeline age-related
Eli LillyNo internal group~34%
Novartis50+ staff~18%
Novo NordiskNo internal group~34%
AbbVieNo (Calico deal ended)~12%
Regeneron10-20 staff~16%
The flywheel

The longevity capital flywheel, with a warning label

  1. Billionaire and VC capital
  2. Elite talent and platforms
  3. Bigger, faster experiments
  4. Credible milestones
  5. Higher valuations, more capital
0.25-0.5%Of global biomedical R&D goes to the biology of aging

About $1-2B a year worldwide, less than a single big drug's Phase III budget. Alzheimer's research alone receives roughly 8x more than the study of aging itself, despite aging being its largest risk factor.

Test yourself

In the chart, Calico ($3.5B) and Altos ($3B) together raised about how much compared with the other five platforms combined?

Eli Lilly and Novo Nordisk have no internal aging group but about 34% of their pipelines are age-related. What does the chapter conclude?

07

No Approved Drug

The real bottleneck

A rounding error

Aging biology is dwarfed by the diseases it causes

Annual research funding by area $B
View the data
Funding
Biology of aging0.5
Children's health7
Rare diseases7
Infectious diseases15
Late-stage aging diseases18

Source: Silver Linings; NIH

Why there is still no drug

Five interlocking barriers

  • Credibility. Decades of over-claiming left the field a snake-oil reputation.
  • No precedent. No regulator has ever approved a drug for aging.
  • No pathway. Aging isn't a recognized indication; no trial guidance exists.
  • No constituency. Patients rally for named diseases, not for 'aging' itself.
  • Capital defaults to disease. So even aging-derived drugs are tested one disease at a time.
The workaround

Alternatives to the impossible mortality trial

Trial endpoints, from hardest to easiest

EndpointDescription
04 All-cause mortalitythe gold standard: unambiguous, but ~30 years and $300M+, effectively impractical.
03 Disease-prevention endpointsone drug delays several age-related diseases; years and $10s-100s M; the FDA is seen as open to this.
02 Functional parametersgrip strength, gait speed, cognition; months to years; no agreed measure yet.
01 Biomarkers & aging clocksblood and epigenetic patterns that predict risk; fast and cheap, but unvalidated.
$144MARPA-H's five-year bet to make aging measurable (2026)

The PROSPR program (up to $144M in contracts to seven teams, announced February 2026) is building an 'intrinsic capacity' score from wearables, blood biomarkers and function tests to predict 20-year outcomes, a possible stand-in for the impossible mortality trial. It plans to test rapamycin, SGLT2 inhibitors and GLP-1s against it.

Sort every claim by evidence

From proven to purely theoretical

Evidence spectrum, from proven to speculative

InterventionEvidence status
Exercise & fitnessmoves mortality, robustly
Statins, SGLT2, GLP-1proven for disease
Rapamycinstrong in mice, human gap
Partial reprogrammingfirst human trial, 2026
Whole-body / cryonicslargely theoretical
The investment case

A genuinely large prize, genuinely guarded

The bull caseThe bear case
Huge market. Slowing aging is worth trillions in GDPNo human proof. Zero approved anti-aging drugs, ever
Real biology. A century of animal proof; tools improving fastLong timelines. Trials take decades; patents do not wait
Rules may bend. ARPA-H, Loyal and new endpoints are emergingHype risk. A field with a long record of over-promising
Early innings. Today's valuations may later look cheapConcentration. A few big failures could set the field back years

Test yourself

Why are aging clocks and blood biomarkers not yet a replacement for the mortality trial?

Why is the biology of aging funded at only about $0.5B a year while late-stage aging diseases get about $18B?

08

Reference

Glossary and sources

We can already slow aging in a mouse and revive a worm frozen for forty-six thousand years. What we cannot yet do is run the trial that would let us sell the cure, and that, not the biology, is the bottleneck.

Reference

Plain-language glossary

TermMeaning
Geroscience hypothesisaging is one shared process behind many diseases; target it once, prevent many.
Hallmarks of aginga twelve-part catalogue of the molecular damage that accumulates with age.
Senescent cella damaged cell that stops dividing but lingers, leaking inflammation ('zombie cell').
Senolytica drug meant to clear senescent cells; promising in mice, unproven in humans.
Partial reprogrammingbriefly applying Yamanaka factors to rejuvenate a cell without erasing its identity.
Rapamycin / mTORan immune drug that slows the cell's growth sensor and extends mouse lifespan.
All-cause mortalitydeath from any cause: the gold-standard but impractical aging endpoint.
Healthspan vs lifespanyears lived in good health, versus total years lived.
Reference

Sources & Further Reading

  • Institute for Health Metrics and Evaluation (IHME): Global Burden of Disease (2023).
  • Lopez-Otin et al.: 'Hallmarks of Aging: An Expanding Universe,' Cell (2013; 2023).
  • NIH Interventions Testing Program: independent mouse lifespan results (2004-2025).
  • Nature: rapamycin and rapamycin + trametinib lifespan studies (2009; 2025).
  • Cochrane Library; Aging Cell: statin, SGLT2 and GLP-1 all-cause mortality analyses.
  • age1: 1st Annual Pharma Aging Report Card (2025).
  • ARPA-H: PROSPR program announcement (2026).
  • Figures marked 'est.' or 'illustrative' are compilations of the above.

Test yourself

A person lives to 90 but has serious illness for the last 20 years. Which statement fits?

What is a senolytic, and what is its current status?

Sources cited

IHME (2023) · Gero · age1 (2025-26) · Gompertz-Makeham law of mortality · ACSM · Cambridge · Science · The Milbank Quarterly · UN/OWID · SSA · Silver Linings · GDP-of-Aging study · Nature · The Evolution of Aging · Cell · Lopez-Otin et al., Cell (2013; 2023) · J. Comparative Physiology B · AnAge, Human Ageing Genomic Resources (Tacutu et al., Nucleic Acids Research, 2018) · Congdon et al., Experimental Gerontology (2001); Ebert, Experimental Gerontology (2008); de Bruin et al., Biology of Reproduction (2004) · Ruby et al., eLife (2018); Keane et al., Cell Reports (2015) · NIH ITP (2004-2025) · Cochrane Library · Aging Cell · UK Biobank · Diabetes Obesity & Metabolism (2014) · Int'l J. Epidemiology (2022) · The Longevity Acceleration Roadmap · Loyal · Life Biosciences (2026) · OPTN · PLOS Genetics · MIT Tech Review · Company disclosures · NIH · National Law Review · How to Design a Clinical Trial for Aging · ARPA-H · Longevity.Technology (Feb 2026) · Loyal press release (Feb 2026) · Fortune (Apr 2026) · Life Biosciences (Jun 2026) · Cure longevity funding tracker (Jul 2026) · ARPA-H PROSPR (2026)

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Research, not investment advice. Figures as of , from the sources cited.

Legal information and disclosures

These are my own views as of the update shown on this page. They can change without notice, and I have no duty to update them. Past performance does not indicate future results, and any investment can lose money.

This is for education only. It is not investment, legal, tax, medical or accounting advice, and it is not an offer to sell or a solicitation to buy any security in any jurisdiction. It does not consider your goals or circumstances.

Figures from company filings, public agencies and other third parties are believed to be reliable, but I have not independently verified them and cannot guarantee them. Forecasts and anything marked as an estimate rest on assumptions that may prove wrong.

Please do not copy or republish this material without my written consent.