Proteome Sciences. AGM Statement.

In continuation of 23855 / 23865.

maxwellsdemon - 20 Jan'05 - 16:10 - 6118 of 23866 (premium)

Jt,

I think this patent application (bar the Intronn patents) could potentially be one of the most important of PRM's patents to date. The assignees names are King's College and PRM. So it is not clear whether PRM have 100% ownership of the rights or if they are shared with King's College.

goatherd - 20 Jan'05 - 16:57 - 6120 of 23866 (premium)


Poolman,

The patent is important, among other reasons, as if it enables us to diagnose Alzheimer's Disease early, and to control or cure it, it could be worth up to $7b a year to us.

Is that important enough for you?

Richard


small crow - 20 Jan'05 - 19:29 - 6127 of 23868

re the patent.

It clearly mentions a whole raft of neurological diseases which I guess are either known or suspects to be connected with the mis-phosphorylation of tau. Included are such as CJD and Down's Syndrome, as well as the obvious candidate of Alzheimers. The patent is about screening techniques, and note that the techniques mentioned include nucleic acid methods as well as proteomic methods, and therapies deriving from these screeing techniques. The mention of these nucleic acid methods paves the way, in my opinion, for Intronn splicing to be used as theraputics in at least some cases, for example, splicing to modify the activity of some of the kinase enzymes. Impossible to properly evaluate, but potentially massive if the screening and therapies work!


2BOB - 20 Jan'05 - 20:50 - 6130 of 23868

From a non patent expert the publication of the tau patent is worthy of note on several points

a) The speed of publication - just over 6 months
b) Why was there no RNS as per the cancer patents if Tau was significant?
c) The publication of the patent can be because PRM want to do a deal in this area soon or perhaps use its publication as a tool to keep others out or force them to pay a licence fee if they are infringing the PRM/IOP patent. It is more likely to be the former, so I am on the lookout for a deal.
d) The way these things usually work IoP KCL will be on the patent because they will have in an agreement assigned the commercialisation rights to PRM for a royalty fee. I have no knowledge that this agreement has been announced. Perhaps jt will. Also unknown to most of us as small crow hints is the detail of the potential linkage back from IoP to Intronn.
e) If this is an important class breakthrough I would not expect all details to be in this patent, but rather other "submarine" patents will already be lodged to fully protect and extend the patent position. They will then surface at the appropriate juncture.
f) Around the time the patent application was lodged (June 04) jt told us on these boards all about the 12 site tau protein breakthrough and PRM's strong patent position. When challenged he was not able to provide any evidence for his claims. I suspect the supporting evidence has now come down the tunnel which shows how close to the inside his information was. But more to the point for those trying to divine the truth in PRM's future path is its accuracy.
g) And last but by no means least, how come maxwellsdemon missed the patent? Stewards inquiry required! Only kiddin' :-)

small crow - 20 Jan'05 - 21:06 - 6132 of 23869

2Bob

I agree (unusually!) that, in this field, this patent should preempt a deal of some kind. What has also been hinted at in the past is that what PRM seem to know about tau and phosphorylation sites may well constitute a 'final common pathway' for many neurological conditions, and this patent reinforces that hint. If they have it right, and my reading of this and other statements is that theraputic principle is not far away, then it could obviously be huge. What is interesting on the Intronn front is that I reckon the wording of this could be large enough to include any competing RNA technologies, such as RNAi, thus stopping any competitor in those fields from trespassing in this particular patch. They have also tried very hard to close all doors on screening technologies, either to be safe or because they have notions on the whole lot of them, depending on the illness? All in all, rather more interesting even than a post from Nelly.

maxwellsdemon - 20 Jan'05 - 21:15 - 6133 of 23869 (premium)

2BOB,

I missed the patent because the WIPO PCT search engine must have a bug in it. :-)

The patent was initially filed 25 June 2003 (the priority date) in GB (not June 2004 as per your post) and procecuted via the WIPO-PCT route. The publication of the patent occurs 18 months after filing. So the fact that the patent was published recently was not down to the company. Apart from the obvious fact this is about 18 months from the initial filing which was under the control of the assignees.

If the company wishes to negotiate a deal in the period prior to publishing but after filing then there is nothing to stop the company revealing the contents of the patent application to other parties. This could be done within or without a non-disclosure agreement.

11) WO 2005/001114
(13) A2


(21) PCT/GB2004/002739

(22) 25 June 2004 (25.06.2004)

(25) English
(26) English

(30) 0314943.2 25 June 2003
(25.06.2003) GB
(43) 06 January 2005 (06.01.2005)



maxwellsdemon - 20 Jan'05 - 21:44 - 6134 of 23869 (premium)


poolman,

This patent application does indeed relate to PRM's Alzheimer's programme. However the patent is worded in such a way that it should cover all the diseases implicated in the modification of the phosphorylation sites of the Tau protein. E.g: frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17), progressive supranuclear palsy (PSP)............

As far as I can make out from an initial read of the claims is the key thing about this patent is that is not protecting a therapeutic cure for these diseases but primarily relates to methods for screening for drugs/substances which may affect the course of any one of the diseases. I have listed some of the independent claims below and from these you should get some idea of what it is that they are trying to protect.

To use some patent jargon; I can most certainly say I am not skilled in the art. So I do not know how novel this invention is or whether these claims will be granted.

But, if the claims are substantially granted, if PRM/King's can enforce the patent and the various novel mechanisms described in the patent are indeed implicated in the tauopathies then they could be in a very strong position.


Claims: 1. Use of casein kinase 1, or a nucleic acid molecule encoding the casein KINASE 1, for screening for candidate compounds which are capable of (a) inhibiting the activity of casein kinase 1 in phosphorylating a tau protein or (b) binding bo casein kinase 1 to inhibit its interaction with a tau protein.

22. A method of screening for substances which are capable of inhibiting the phosphorylation of a tau protein by casein kinase 1 (CK1), wherein the tau protein comprises one or more phosphorylation sites, the method comprising: (a) contacting at least one candidate substance, the tau protein and casein kinase 1 under conditions in which the casein kinase 1 is capable of phosphorylating the site (s) of the tau protein in the absence of the candidate substance; (b) determining whether, and optionally the extent to which, the candidate substance inhibits the phosphorylation of the tau protein at one or more sites of the tau protein by casein kinase 1; and, (c) selecting the candidate substance which inhibits phosphorylation of the tau protein at one or more of the sites

49. Use of fyn, or a nucleic acid molecule encoding fyn, for screening for candidate compounds which are capable of (a) inhibiting the activity of fyn in phosphorylating a tau protein at a position corresponding to Y394 or (b) binding to fyn to inhibit its interaction with a tau protein AT Y394.

48. A method of screening for substances which are capable of inhibiting the phosphorylation of a tau protein AT A phosphorylation site at position Y394 by fyn, the method comprising: (a) contacting at least one candidate substance, the tau protein and fyn under conditions in which the fyn is capable of phosphorylating position Y394 of the tau protein in the absence of the candidate substance ; (b) determining whether, and optionally the extent to which, the candidate substance inhibits the phosphorylation of the tau protein at position Y394 of the tau. protein by fyn; and, (c) selecting the candidate substance which inhibits phosphorylation of the tau protein at position Y394.

49. A method of screening for substances which are capable of inhibiting phosphorylation by a kinase at one or more of the site (s) of a tau protein selected from the group consisting of S68, T69, T71, (T111/S113), S191, S258, S289, (T414/S416), T427, S433, S435 and Y394, the method comprising: (a) contacting at least one candidate substance, a tau protein which comprises one or more of the phosphorylation sites and a kinase which is capable of phosphorylating the tau protein under conditions in which the kinase is capable of phosphorylating one or more of the sites of the tau protein in the absence of the candidate substance; (b) determining whether, and optionally the extent to which, the candidate substance inhibits the phosphorylation of the tau protein at one or more sites of the tau protein; and, (c) selecting the candidate substance which inhibits phosphorylation of the tau protein at one or more of the sites.

50. A method of screening for substances which are capable of promoting dephosphorylation of a tau protein by a phosphatase at one or more of the site (s) of a tau protein selected from the group consisting of S68, T69, T71, (T111/S113), S191, S258, S289, (T414/S416), T427, S433, S435 and Y394, the method comprising: (a) contacting at least one candidate substance, a tau protein comprising one or more the phosphorylation site and a phosphatase which is capable of dephosphorylating the tau protein under conditions in which the phosphatase is capable of dephosphorylating the site (s) of the tau protein in the absence of the candidate substance; (b) determining whether, and optionally the extent to which, the candidate substance promotes the dephosphorylation of the tau protein at one or more sites of the tau protein; and, (c) selecting the candidate substance which promotes dephosphorylation of the tau protein at one or more of the sites