Tom Grahn Kristiina GrahnEritoCap LtdAX 22930 Fiskö, Åland, Finland+358 500 828486tpgrahn@gmail.com

Fall 2015

To Whom It May Concern

In Brief –The Competitive Advantage of DEA

DEA( d-eritadenine ) is a multitherapeutic bioactive small molecule ( 252 g/mol ) bio-synthetized as a secondary metabolite only by the mycelium of Lentinula edodes, the shiitake. Hence 50 – 60 t of DEA is consumed annually with the fruitbody, mostly in the Far East. It was discovered in Japan in 1966. Only recently its science was revealed ( 1993 – 1998 ) by Kimio Sugiyama. Its science and technology commercial platform has been revealed by me since 1999 until date. Through or family company we own the IP for the United States on the use of DEA in primary and secondary foods, the master patent.

In Tokyo in 1993 I decided that One Day I will research d-eritadenine, DEA. That day came in spring of 1999. The IP priority date is November 24. 1999. The work I have performed have been done for 15 years now, and it still continues. I have done all this in order to find the commercial partnerowner for DEA. Therefore I write to you today

The competitive advantage of DEA

Let me define the competition of DEA leading to the competitive advantage I have seen for more than 15 years.

The graphLeft upper corner: CARDIOVASCULAR AND ANTIATHEROGENICSugiyama in 1993 started his work with DEA as a soy protein specialist at Shizuoka University. He wanted to explore the potens of similar ingredients to soy mechanism. He established the theorem that carries his name: All ingredients that reduce PC/PE are hypocholesteremic. I deducted the endogenous reduction mechanism of LDL receptor increase. Later in 2008 Nestle researchers in South Korea proved it. The causality of cardiovascular and antiatherogenic therapy on cognitive performance is proven. LDL and HDL are EFSA biomarkers ( European Food Safety Authority, ie EU equal to FDA )

Right upper corner: COGNITIVE HCY, homocysteine, is an amino acid that has no other function than to rotate the One Carbon Ring ( +CH3 – CH3, methyldonoring, methylacceptoring ). The know-how platform of HCY is recent, only some 15 – 20 years. It was created when the “ cholesterol-doctrin “ solved most cardiovascular matters, and Kilmer McCully was its first victim. The graph was created based on EFSA ( European Food Safety Authority ) biomarkers ( as red ). HCY is an EFSA biomarker.

Tom Grahn 1999-2012 Finland +358 500 828486 tpgrahn@gmail.com

USE OF DEAGLOBALLY

PROTECTEDCAUSALITY PROVEN

DEA humandaily dose 30 mg

EFSA: HCY biomarker

EFSA: LDL and HDL biomarkers;

Sugiyama Theoremall PC/PE reducers

are cholesterolreducers!!

EFSA: blood pressure& platelet activity

biomarkers

State of methylation;

new biomarker

a kinetic fact in the One C Ring

The mostpotent

Cheon 2008 Dr thesis

Glapski 2004 Dr thesis

SAHHinhibition

Right bottom corner: MEMBRANE FLUIDITY AND BLOOD TONICINGThe 2008 Dr thesis of Yewon Cheon fulfilled my graph. It was already known that DEA starting at SAH hydrolas ( SAHH ) inhibition in the One Carbon Ring first reduces the PC/PE ratio ending up in delta6desaturase downgrading. Ms Cheon could show that this

kinetic action was mediated by SREBP 1 ( sterol regulatory binding protein 1 ). The EFSA biomarkers that DEA influence via increased membrane fluidity and blood tonicing are blood pressure and platelet activity

Left bottom corner: EPIGENETICWhen I started my DEA work tour in 1999 the epigenetic phenomenon was hardly known. I ran into it in my 2008 work on transposon detection business plan for Boreal Ltd in Finland ( moving elements, Nobel prize 1982, Barbara McLintock ). The DEA circle as presented in the graph was closed. Pragmatically expressed the One C ring is rotating via CH3 donoring and acceptoring. The folatedependent and folateindependent two effects on HCY reduction and is speeding up the ring rotation. The third less know effect on HCY reduction is SAH hydrolas inhibition. Kinetically DEA decrease HCY and hence slows down the One C Ring rotation. Glapski’s Dr thesis in France 2004 was highy revealing in showing the feedback inhibition control between SAH and SAM. Epigenetism is not yet an EFSA accepted biomarker, but it will become.

The Competitive Advantage of DEA is its multitherapy. The commercial competition of DEA is by large and only singletherapeutic. EFSA has so far never approved an ingredient with multitherapeutic effect. When I planned, designed and worked out the Clinical trial and later, the Clinical test, programme, the core of these was to establish the true multitherapeutic effects of DEA. One competive advantage is also its bioactive action already at small human doses ie 30 mg. Sterols and –derivaties requires 2.5 – 3 g. Soy protein 20 g

Dear Reader,I offer you all what I know and have on DEA and its USA IP for 150 000 EUR. The price is face cost value of 15 years of work. I can prove that the price tag of DEA has been accepted at 1 MEUR level by several giants and specialist companies through the years. My stepping stone essentially has been the lack of human clinical testing, that Danisco was the first to demand. Later joiners were Nestle, Unilever, DSM, Martek, Provexis, Bunge etc, etc. A huge USA one cannot be mentioned. And that is not Pfizer.

I confirm to you: DEA is a sleeping beauty.

yours,

Tom Grahn, senior, Tech Lic, running for Dr ScFinland