R&RHashman
Well-Known Member
might be brain damage from bad co-solvent like Freon. lol im sry oilmkr you are a fun read
man this stuff is always funny
man this stuff is always funny
Real Chemistry
- Thread starter oilmkr420
- Start date
oilmkr420
Active Member
US 8,586,767 B2
METHOD FOR TREATMENT OF HIV AND DISEASES OF IMMUNE DYSREGULATION
Craig Rick Travis, South Miami, Fla. (US)
Filed by Craig Rick Travis, South Miami, Fla. (US)
Filed on Jan. 23, 2012, as Appl. No. 13/355,676.
Application 13/355,676 is a continuation in part of application No. 11/978,318, filed on Oct. 29, 2007, abandoned.
Application 11/978,318 is a continuation in part of application No. 11/327,693, filed on Jan. 5, 2006, abandoned.
Application 11/327,693 is a continuation of application No. 10/328,242, filed on Dec. 22, 2002, granted, now 7,105,685.
Application 10/328,242 is a continuation of application No. 09/928,683, filed on Aug. 13, 2001, granted, now 6,566,560.
Application 09/928,683 is a continuation in part of application No. 09/533,386, filed on Mar. 22, 2000, granted, now 6,274,635.
Claims priority of provisional application 60/125,674, filed on Mar. 22, 1999.
Claims priority of provisional application 60/151,595, filed on Aug. 30, 1999.
Prior Publication US 2012/0122917 A1, May 17, 2012
Int. Cl. C07D 311/80 (2006.01); A01N 43/16 (2006.01)
U.S. Cl. 549—390 [514/454]7 Claims
1. A method of treatment of Human Immunodeficiency Virus (HIV) by administering to a subject in need thereof a composition comprising a cannabinoid derivative, wherein said cannabinoid derivative is (6aR,10aR)-1-methoxy-6,6,9-trimethyl-3-(2-methyloctan-2-yl)-6a,7,10,10a-tetrahydrobenzo[c]chromene (L-759633) having the formula:
METHOD FOR TREATMENT OF HIV AND DISEASES OF IMMUNE DYSREGULATION
Craig Rick Travis, South Miami, Fla. (US)
Filed by Craig Rick Travis, South Miami, Fla. (US)
Filed on Jan. 23, 2012, as Appl. No. 13/355,676.
Application 13/355,676 is a continuation in part of application No. 11/978,318, filed on Oct. 29, 2007, abandoned.
Application 11/978,318 is a continuation in part of application No. 11/327,693, filed on Jan. 5, 2006, abandoned.
Application 11/327,693 is a continuation of application No. 10/328,242, filed on Dec. 22, 2002, granted, now 7,105,685.
Application 10/328,242 is a continuation of application No. 09/928,683, filed on Aug. 13, 2001, granted, now 6,566,560.
Application 09/928,683 is a continuation in part of application No. 09/533,386, filed on Mar. 22, 2000, granted, now 6,274,635.
Claims priority of provisional application 60/125,674, filed on Mar. 22, 1999.
Claims priority of provisional application 60/151,595, filed on Aug. 30, 1999.
Prior Publication US 2012/0122917 A1, May 17, 2012
Int. Cl. C07D 311/80 (2006.01); A01N 43/16 (2006.01)
U.S. Cl. 549—390 [514/454]7 Claims
1. A method of treatment of Human Immunodeficiency Virus (HIV) by administering to a subject in need thereof a composition comprising a cannabinoid derivative, wherein said cannabinoid derivative is (6aR,10aR)-1-methoxy-6,6,9-trimethyl-3-(2-methyloctan-2-yl)-6a,7,10,10a-tetrahydrobenzo[c]chromene (L-759633) having the formula:
oilmkr420
Active Member
U.S. Patent Documents
2012/0289589November 2012Travis
Other References
Gareau et al. Bioorganic & Medicinal Chemistry Letters (1996), 6(2), 189-94. cited by examiner .
Galiegue et al., Eur. J. Biochem. 1995, 232, 54-61. cited by examiner .
Noe et al., "Cannabinoid receptor agonists enhance syncytia formation in MT-2 cells infected with cell free HIV-1MN," Adv. Exp Med Biol. 1998, 437:223-9. cited by applicant .
Specter et al. "Delta-9-tetrahydrocannabinol augments murine retroviral induced immunosuppression and infection," Int. J. Immunopharmac., vol. 13, No. 4, pp. 411-417, 1991. cited by applicant .
Solomon, J. et al. ; Effect of delta -9-tetrahydrocannabinol on uterine and vaginal cytology of ovariectomized rats; published on Mar. 4, 1977 and retrieved on Jun. 10, 2013. cited by applicant .
Huff, "HIV Protease: A novel chemotherapeutic target for AIDS", Journal of Medicinal Chemistry (Aug. 1991) 34(
: 2305-2314. cited by applicant .
Huffman et al., "3-(1', 1'-dimethylbutyl)-1-deoxy-D8-THC and related compounds: Synthesis of selective ligands for the CB2 receptor", Bioorganic & Medicinal Chemistry (1999) 7: 2905-2914. cited by applicant.
Primary Examiner: Chandrakumar; Nizal
Attorney, Agent or Firm:Novak Druce Connolly Bove + Quigg LLP
Parent Case Text
CROSS REFERENCE TO RELATED APPLICATIONS
This is a continuation-in-part of U.S. patent application Ser. No. 11/978,318, filed Oct. 29, 2007 now abandoned, which is a continuation-in-part of U.S. patent application Ser. No. 11/327,693 (now Abandoned), filed on Jan. 5, 2006, which is a continuation of U.S. patent application Ser. No. 10/328,242 (now U.S. Pat. No. 7,105,685), filed Dec. 22, 2002, which is a continuation of application Ser. No. 09/928,683 (now U.S. Pat. No. 6,566,560) filed on Aug. 13, 2001, which is a continuation-in-part of U.S. patent application Ser. No. 09/533,386 (now. U.S. Pat. No. 6,274,635) filed on Mar. 22, 2000, which claims priority to U.S. provisional patent application Nos. 60/125,674 and 60/151,595 filed on Mar. 22, 1999 and Aug. 30, 1999, respectively.Claims
I claim:
1. A method of treatment of Human Immunodeficiency Virus (HIV) by administering to a subject in need thereof a composition comprising a cannabinoid derivative, wherein said cannabinoid derivative is (6aR,10aR)-1-methoxy-6,6,9-trimethyl-3-(2-methyloctan-2-yl)-6a,7,10,10a-t- etrahydrobenzo[c]chromene (L-759633) having the formula: ##STR00029##
2. A method of treating diseases of immune dysfunction which are a result of infectious origin comprising Human Immunodeficiency Virus (HIV), or influenza virus (Type A and B) infections using said cannabinoid derivative of claim 1.
3. The use of the cannabinoid derivative of claim 1 in preparing a medicament for treating a disease selected from the group consisting of: HIV, feline immunodeficiency virus (FIV) and simian immunodeficiency virus (SIV) disease, comprising incorporating the cannabinoid derivative of claim 1 into a pharmaceutically acceptable composition comprising a carrier, wherein the cannabinoid derivative of claim 1 is in an amount effective for indirect inhibition of viral replication through attenuation of an immune response which deprives the virus of the signals required by the virus and disrupts the pathways required by the virus for replication, resulting in slowing the progression of said disease.
4. The use of the cannabinoid derivative of claim 1 in preparing a medicament for treatment of a disease selected from the group consisting of: HIV, SIV and FIV disease, comprising incorporating the cannabinoid derivative of claim 1 into a pharmaceutically acceptable composition comprising a carrier and formulating the composition for vaginal or systemic delivery, wherein the cannabinoid derivative of claim 1 is in an amount effective for improving barrier function of vaginal mucosa by strengthening the integrity of tight junctions which bind vaginal epithelial cells together, by increasing the number of layers of the cells, and by disruption of the immune response required by the viruses for transmission as mediated through constitutive expression of CB2 receptors on vaginal epithelial cells and interaction of the CB2 receptors with immune cells.
5. A method of treating transmission of Human Immunodeficiency Virus (HIV) by administering to a subject in need thereof a composition comprising a cannabinoid derivative, wherein said cannabinoid derivative is (6aR,10aR)-1-methoxy-6,6,9-trimethyl-3-(2-methyloctan-2-yl)-6a,7,10,10- a-tetrahydrobenzo[c]chromene (L-759633) having the formula: ##STR00030##
6. The method of claim 5, wherein the composition is administered to mucosal tissue in an amount effective for retarding uptake of the HIV through the mucosal tissue.
7. The method of claim 6, wherein the mucosal tissue is vaginal mucosal tissue and the composition is administered systemically or topically to the vagina.Description
BACKGROUND OF THE INVENTION
The retroviral Human Immunodeficiency Viruses (HIV) 1 and 2 are the most common causative agents of AIDS. Through a portion of a viral envelope protein (gp120), HIV binds specifically and with high affinity to the CD4 molecule on T-lymphocytes. Following binding, the virus fuses with the cell membrane and is internalized. Within the cell, it produces a reverse transcriptase which transcribes its genomic RNA to DNA. The reverse HIV transcript is then integrated into the cellular DNA where it exists for the life of the cell as a "provirus." The provirus can remain latent for an indefinite period of time, or it can be "activated" to transcribe mRNA and genomic RNA, leading to protein synthesis, assembly, new virion formation, budding of virus from the cell surface, and cell death.
While the precise events triggering activation are poorly understood, they appear to lead to liberation or production of endogenous cellular factors that interact with the HIV genome to promote translation. In this regard, binding of cellular SP1 to the HIV promoter (which contains several tandem SP1 consensus binding sites) is needed for high-level transcription of the latent HIV genome. Additionally, NF.kappa.B functions as a potent transcriptional activator when it binds to one or two (depending on the HIV strain) consensus binding sites in the HIV enhancer, which is adjacent to the promoter. The transcription factors CREB/ATF, NF-AT, and AP1 also potentiate HIV transcription. As for all retroviruses, the structural and enzymatic gag, pol and env gene products are produced when the provirus is activated. HIV first transcribes gag-pol as a fusion protein which is ultimately cleaved by the HIV protease enzyme to yield the (nature viral proteins. HIV also employs additional regulatory proteins (specifically the tat and rev gene products) as transcriptional enhancers to induce high levels of gene expression. Nef is another HIV gene that modulates viral replication levels.
While the set of factors triggering active viral replication remains only partially understood, some of them include heat shock, ultraviolet radiation, regulatory proteins of other (e.g., superinfecting) viruses, inflammatory cytokines (e.g., IL1, IL2, IL4, IL6, IL10, Tumor Necrosis Factor a (TNF.alpha.), Platelet Activating Factor, Interferon y (IFN.gamma.)), and Nitric Oxide. Many of these factors are T-cell activators (e.g., they precipitate cell cycling and clonal expansion of T-cell populations), and they are released by many B-cells in direct response to infectious agents (such as HIV). Such factors also trigger intracellular signaling events promoting the production of NF.kappa.B and its dissociation from its inhibitor (IkB). Active NF.kappa.B is a DNA binding protein activating the transcription of many cellular genes, and also the HIV genome. In this regard, cytokines such as TNF .alpha. and IL-1 augment NF.kappa.B activity in cultured T-cells.
Some cells harboring the provirus express HIV gp41, gp120
2012/0289589November 2012Travis
Other References
Gareau et al. Bioorganic & Medicinal Chemistry Letters (1996), 6(2), 189-94. cited by examiner .
Galiegue et al., Eur. J. Biochem. 1995, 232, 54-61. cited by examiner .
Noe et al., "Cannabinoid receptor agonists enhance syncytia formation in MT-2 cells infected with cell free HIV-1MN," Adv. Exp Med Biol. 1998, 437:223-9. cited by applicant .
Specter et al. "Delta-9-tetrahydrocannabinol augments murine retroviral induced immunosuppression and infection," Int. J. Immunopharmac., vol. 13, No. 4, pp. 411-417, 1991. cited by applicant .
Solomon, J. et al. ; Effect of delta -9-tetrahydrocannabinol on uterine and vaginal cytology of ovariectomized rats; published on Mar. 4, 1977 and retrieved on Jun. 10, 2013. cited by applicant .
Huff, "HIV Protease: A novel chemotherapeutic target for AIDS", Journal of Medicinal Chemistry (Aug. 1991) 34(
: 2305-2314. cited by applicant .Huffman et al., "3-(1', 1'-dimethylbutyl)-1-deoxy-D8-THC and related compounds: Synthesis of selective ligands for the CB2 receptor", Bioorganic & Medicinal Chemistry (1999) 7: 2905-2914. cited by applicant.
Primary Examiner: Chandrakumar; Nizal
Attorney, Agent or Firm:Novak Druce Connolly Bove + Quigg LLP
Parent Case Text
CROSS REFERENCE TO RELATED APPLICATIONS
This is a continuation-in-part of U.S. patent application Ser. No. 11/978,318, filed Oct. 29, 2007 now abandoned, which is a continuation-in-part of U.S. patent application Ser. No. 11/327,693 (now Abandoned), filed on Jan. 5, 2006, which is a continuation of U.S. patent application Ser. No. 10/328,242 (now U.S. Pat. No. 7,105,685), filed Dec. 22, 2002, which is a continuation of application Ser. No. 09/928,683 (now U.S. Pat. No. 6,566,560) filed on Aug. 13, 2001, which is a continuation-in-part of U.S. patent application Ser. No. 09/533,386 (now. U.S. Pat. No. 6,274,635) filed on Mar. 22, 2000, which claims priority to U.S. provisional patent application Nos. 60/125,674 and 60/151,595 filed on Mar. 22, 1999 and Aug. 30, 1999, respectively.Claims
I claim:
1. A method of treatment of Human Immunodeficiency Virus (HIV) by administering to a subject in need thereof a composition comprising a cannabinoid derivative, wherein said cannabinoid derivative is (6aR,10aR)-1-methoxy-6,6,9-trimethyl-3-(2-methyloctan-2-yl)-6a,7,10,10a-t- etrahydrobenzo[c]chromene (L-759633) having the formula: ##STR00029##
2. A method of treating diseases of immune dysfunction which are a result of infectious origin comprising Human Immunodeficiency Virus (HIV), or influenza virus (Type A and B) infections using said cannabinoid derivative of claim 1.
3. The use of the cannabinoid derivative of claim 1 in preparing a medicament for treating a disease selected from the group consisting of: HIV, feline immunodeficiency virus (FIV) and simian immunodeficiency virus (SIV) disease, comprising incorporating the cannabinoid derivative of claim 1 into a pharmaceutically acceptable composition comprising a carrier, wherein the cannabinoid derivative of claim 1 is in an amount effective for indirect inhibition of viral replication through attenuation of an immune response which deprives the virus of the signals required by the virus and disrupts the pathways required by the virus for replication, resulting in slowing the progression of said disease.
4. The use of the cannabinoid derivative of claim 1 in preparing a medicament for treatment of a disease selected from the group consisting of: HIV, SIV and FIV disease, comprising incorporating the cannabinoid derivative of claim 1 into a pharmaceutically acceptable composition comprising a carrier and formulating the composition for vaginal or systemic delivery, wherein the cannabinoid derivative of claim 1 is in an amount effective for improving barrier function of vaginal mucosa by strengthening the integrity of tight junctions which bind vaginal epithelial cells together, by increasing the number of layers of the cells, and by disruption of the immune response required by the viruses for transmission as mediated through constitutive expression of CB2 receptors on vaginal epithelial cells and interaction of the CB2 receptors with immune cells.
5. A method of treating transmission of Human Immunodeficiency Virus (HIV) by administering to a subject in need thereof a composition comprising a cannabinoid derivative, wherein said cannabinoid derivative is (6aR,10aR)-1-methoxy-6,6,9-trimethyl-3-(2-methyloctan-2-yl)-6a,7,10,10- a-tetrahydrobenzo[c]chromene (L-759633) having the formula: ##STR00030##
6. The method of claim 5, wherein the composition is administered to mucosal tissue in an amount effective for retarding uptake of the HIV through the mucosal tissue.
7. The method of claim 6, wherein the mucosal tissue is vaginal mucosal tissue and the composition is administered systemically or topically to the vagina.Description
BACKGROUND OF THE INVENTION
The retroviral Human Immunodeficiency Viruses (HIV) 1 and 2 are the most common causative agents of AIDS. Through a portion of a viral envelope protein (gp120), HIV binds specifically and with high affinity to the CD4 molecule on T-lymphocytes. Following binding, the virus fuses with the cell membrane and is internalized. Within the cell, it produces a reverse transcriptase which transcribes its genomic RNA to DNA. The reverse HIV transcript is then integrated into the cellular DNA where it exists for the life of the cell as a "provirus." The provirus can remain latent for an indefinite period of time, or it can be "activated" to transcribe mRNA and genomic RNA, leading to protein synthesis, assembly, new virion formation, budding of virus from the cell surface, and cell death.
While the precise events triggering activation are poorly understood, they appear to lead to liberation or production of endogenous cellular factors that interact with the HIV genome to promote translation. In this regard, binding of cellular SP1 to the HIV promoter (which contains several tandem SP1 consensus binding sites) is needed for high-level transcription of the latent HIV genome. Additionally, NF.kappa.B functions as a potent transcriptional activator when it binds to one or two (depending on the HIV strain) consensus binding sites in the HIV enhancer, which is adjacent to the promoter. The transcription factors CREB/ATF, NF-AT, and AP1 also potentiate HIV transcription. As for all retroviruses, the structural and enzymatic gag, pol and env gene products are produced when the provirus is activated. HIV first transcribes gag-pol as a fusion protein which is ultimately cleaved by the HIV protease enzyme to yield the (nature viral proteins. HIV also employs additional regulatory proteins (specifically the tat and rev gene products) as transcriptional enhancers to induce high levels of gene expression. Nef is another HIV gene that modulates viral replication levels.
While the set of factors triggering active viral replication remains only partially understood, some of them include heat shock, ultraviolet radiation, regulatory proteins of other (e.g., superinfecting) viruses, inflammatory cytokines (e.g., IL1, IL2, IL4, IL6, IL10, Tumor Necrosis Factor a (TNF.alpha.), Platelet Activating Factor, Interferon y (IFN.gamma.)), and Nitric Oxide. Many of these factors are T-cell activators (e.g., they precipitate cell cycling and clonal expansion of T-cell populations), and they are released by many B-cells in direct response to infectious agents (such as HIV). Such factors also trigger intracellular signaling events promoting the production of NF.kappa.B and its dissociation from its inhibitor (IkB). Active NF.kappa.B is a DNA binding protein activating the transcription of many cellular genes, and also the HIV genome. In this regard, cytokines such as TNF .alpha. and IL-1 augment NF.kappa.B activity in cultured T-cells.
Some cells harboring the provirus express HIV gp41, gp120
Sirdabsalot462
Well-Known Member
oilmkr420
Active Member
I thou
I thought you knew that freon evaporated cleaner than butane leaving less residue. But how the fuck would you guys know as you wish you could get some. Ahhh, too bad.
Twitch
Well-Known Member
but it doesn't,,,,,
oilmkr420
Active Member
From someone who employs the use of co-solvents, you fuckin wish too!
R&RHashman
Well-Known Member
yeah I winterize with everclear. still safer then Freon.
oilmkr420
Active Member
Have you even seen the msds for ethanol? It shocked the shit out of me to see how safe it wasn't. However dangerous or accepted it is or isn't, the msds had me scratching my noodle. The shit's the worst chemical I deal w and the proof was in o-ring failures the extreme low temperatures in combination w alcohol make a poor mans liquid nitrogen, but it causes failure w many different materials I hadn't a clue were a source of contamination in some instances in a few batches. Ethanol is by far more accepted to use than freon, but after trying both, it's hard to discredit the facts behind using them. It leaves impressive results and purges easy.
Blunter the kid
Well-Known Member
Mind posting a video of your method of winterizing using freon?
I have a hard time believing that your method of winterization causes more waxes to drop out of solution.
At least explain your process, everyone seems to discredit you at every turn, why do you not try and make a coherent argument defending yourself..?
It makes you look arrogant trying to claim fame to something with no real scientific basis other than the fact that freon is colder at atmospheric pressure than iced ethanol is.
Anyways I'd like to hear an argument if u would take the time to write one up.
Also that part about ethanol is absolutely ridiculous... Ethanol is not a dirty chemical... Most of the production of ethanol is a produced via a biosynthetic reaction of SUGAR + WATER + YEAST all three of which are consumed everyday, at no time does the alcohol have a chance to pickup impurities during the production process unless the manufacturer adds them, as in the case of denatured ethanol... If your unhappy after reading the msds of that specific brand of ethanol (probably denatured) then you could go buy food grade and dry it over MgSO4, or take denatured and distill the vapor through activated charcoal to remove anything from the ethanol you wouldn't want..
Last edited:
Frenchy Cannoli
Well-Known Member
This is the thread I remember you from Oilmkr. You do not have any ego problem that's a fact.
Yo what's up w guys? Does anybody do shit big up there, got their shit together, and willing to be the next big wax competitor out there? It takes cash. If you got that and desire to learn the biz, then don't think Apex or Eden as the only pros in the biz, as I had grabbed both companies attention, and a couple clients as I proved myself an expert in this field, w much to contribute to how one can manipulate carbon dioxide to be predictable and repeatable all the time. I would love to compare extracts w Eden,Apex, JYNdustries, and Hashmasta kut as my dedicated works shows effort well spent and I put my confidence as I am aware of their methods and I feel like I got major edge even on these pros and know it alls. So people esp growers in NorCal, HMU or PM me as to invest the minimum to have me go to you, or come to me. Either place I have most advantage as you guys at best are working w MZ12 and most likely under purged. I talk a lot of shit, but easily back it up. Hope to hear from an eager reader.
But seriously?????
Yo what's up w guys? Does anybody do shit big up there, got their shit together, and willing to be the next big wax competitor out there? It takes cash. If you got that and desire to learn the biz, then don't think Apex or Eden as the only pros in the biz, as I had grabbed both companies attention, and a couple clients as I proved myself an expert in this field, w much to contribute to how one can manipulate carbon dioxide to be predictable and repeatable all the time. I would love to compare extracts w Eden,Apex, JYNdustries, and Hashmasta kut as my dedicated works shows effort well spent and I put my confidence as I am aware of their methods and I feel like I got major edge even on these pros and know it alls. So people esp growers in NorCal, HMU or PM me as to invest the minimum to have me go to you, or come to me. Either place I have most advantage as you guys at best are working w MZ12 and most likely under purged. I talk a lot of shit, but easily back it up. Hope to hear from an eager reader.
But seriously?????
Blunter the kid
Well-Known Member
I couldn't tell whether you were being sarcastic or not :3
Frenchy Cannoli
Well-Known Member
You actually have to read the post on his thread to get it, I know!
Blunter the kid
Well-Known Member
The whole thread seems to be people putting down his ideas, nobody even tried to dispute what he was saying everyone just dismissed him.
After reading all that, I don't think he's arrogant but for whatever reason the people on this forum just hate on him.
Still he doesn't really try to dispute anything with any of them.
Frenchy Cannoli
Well-Known Member
I do not know what he does, how good he is or the level of his expertise if any, it is just the way he introduced himself, (see above quote) and to whom he is trying to introduce himself.
On the other hand he seems to be known on RIU and not very much appreciated, his attitude could be the source.
On the other hand he seems to be known on RIU and not very much appreciated, his attitude could be the source.