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” LET FOOD BE YOUR EPIGENETIC MEDICINE

”*Prospectus by Tom Grahnon DEA for US interestedparties , November 2015

•Clinical Epigenetics Journal 2015, 7:33

Tom Grahn, Finland, +358 500 828486, tpgrahn@gmail.com

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DEA, d-eritadenine, originates in Japan. I took it to the West.

The mother, the mycelium, produces the 2ndary metabolite DEA for the daughter , the fruitbody. which we eat

.

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DEA is the very first multitherapeutic bioactive epigenetic food ingredient for a long time.

The entrepeneur at cloning, and the cloning cuts

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DEA is the secondary metabolite biosynthetizised by the mycelium, in

this case, the DEA superstrainLeft two days old clones, at the right in submerged

cultivation

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The success can be seen in the bottle!

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HCYSAHH PC ~PE

SAH SAM

CARDIOVASCULARIMPACT &

ANTIATHEROGENIC ANTIATHEROSCLEROTIC

COGNITIVEIMPROVEMENTS

EPIGENETICMETHYLATION

STATE CONTROL ENHANCED MEMBRANE FLUIDITY

ω3 BOOSTING

18:218:3

CATABOLISMVia SREBP 1 Δ6D

+CH3 -CH3

Tom Grahn All rights reserved +358 500 828486 tpgrahn@gmail.com Finland Nov 2015

USE OF DEAGLOBALLY PROTECTED

DEA humandaily dose30 mg

Phospholipidic

modification !

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The DEA KEY window is… DEA is a phosphilipidic modifier and

down-regulates PC/PE. This in turn deactivates SREBP 1 ( Yewon Cheon Dr Thesis 2008 ) which is a key catalyser in fatty acid metabolism. Via the SREBP 1 the D6D ( delta-6desaturase ) anabolism is inhibited and w3 boosted. SAHH is kinetically reducing HCY. The One Carbon Ring rotation is regulated by the +CH3/-CH3 state of SAH/SAM. DEA is epigenetic “ medicine “The multitherapeutic window of DEA is governed by these facts

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The discovery history behind the DEA KEY window

* DEA was discovered in Japan in 1966 and Tanabe and Fujisawa was fiercely competing for 10 years.

* DEA as a potent SAH hydrolas inhibitor was discovered in 1982 by Vortruba and Holy

* The Sugiayama theorem goes back to early 1990’s: ” PC/PE reducers are always hypocholestermic ”

* Dr Shimada revealed the sequential nutrition kinetics of DEA over PC/PE and fatty acid catabolism in 2003

* Dr Cheon 2008: ”SREBP 1 is the transcriptional regulator and its activity is regulated by membrane PC/PE ratio”

* It is only recently the understanding of epigenetics and nutrition versus state of methylation is paying off.

* All this, and more, is included in this S&T platform

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DEASCDEASC stands for DEA supply chain•A fermentation manual was performed in 2010• Separation of DEA is performed by HPLC since 2011• For pharma purposes DEA can be synthetisized

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How DEA binds to SAHHDr Cedric Glapski in 2004

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TAKEN TOGETHER…

Taken together, these 10 pages offer clearly the following

therapeutic window: 1. Hypocholesteremic due to PC/PE, SREBP1 and D6D

2. Hypohomocysteinemic due to SAHH inhibition an kinetic fact

3. EFA boosting and membrane fluidity

due to D6D inhibition 4. Epigenetic control due to SAM/SAH

regulation 5. Vascular cognitive effects due to the

above four

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FOSHU, GRAS AND NOVEL D-eritadenine is

FOSHU in Japan GRAS in the USA Novel Food in Europe

EFSA biomarkers are ( European Food Safety Authority)

LDL and HDL HCY Blood pressure and platelet activity

DEA impacts all these and is multitherapeutic in pharmafood sence

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US PATENTS USA, 9.11 2004 USP 6,814,975 B1 24.11 2000 Granted

Exp 19.3 2021

USA, 27.6 2006 USP 7,067,146 24.11 2000Granted

Exp 20.11 2020 The patents are maintained and owned by EritoCap Ltd, the Grahn company

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All this is …Available through my company EritoCap Ltd, FI 1469575-5 Finland, trade registered 734.081, domicile Turku, Finland.Tom Grahn:

I sell all and participate in commercialisation at face cost of 15 yrs of work.