Marijuana Sector Positioned to Move Higher as FDA Reviews Drug’s Status
Jun 30, 2014 (ACCESSWIRE via COMTEX) — WHITEFISH, MT / June 30, 2014 / The Marijuana Index(TM) traded marginally lower last week after MedBox Inc. MDBX -2.31{92d3d6fd85a76c012ea375328005e518e768e12ace6b1722b71965c2a02ea7ce} and CannaVEST Corp.’s CANV -16.40{92d3d6fd85a76c012ea375328005e518e768e12ace6b1722b71965c2a02ea7ce} moves lower offset GW Pharmaceuticals plc’s GWPH -7.95{92d3d6fd85a76c012ea375328005e518e768e12ace6b1722b71965c2a02ea7ce} modest gains.
Top gainers included Tauriga Sciences Inc. TAUG -8.18{92d3d6fd85a76c012ea375328005e518e768e12ace6b1722b71965c2a02ea7ce} , which jumped more than 60{92d3d6fd85a76c012ea375328005e518e768e12ace6b1722b71965c2a02ea7ce} after saying that it remains on track with its Honeywood acquisition to commercial products in the medicinal cannabis sector, and Vape Holdings Inc. VAPE -7.69{92d3d6fd85a76c012ea375328005e518e768e12ace6b1722b71965c2a02ea7ce} , which jumped more than 40{92d3d6fd85a76c012ea375328005e518e768e12ace6b1722b71965c2a02ea7ce} after reporting results from the soft launch of its e-commerce website HiveCeramics.com last week. The largest decliners included Easton Pharmaceuticals Inc. EAPH -10.67{92d3d6fd85a76c012ea375328005e518e768e12ace6b1722b71965c2a02ea7ce} , which fell nearly 20{92d3d6fd85a76c012ea375328005e518e768e12ace6b1722b71965c2a02ea7ce} last week.
Cannabis regulatory initiatives and news were mixed last week. While the United Nations warned about a rise in cannabis-related medical cases following legalization efforts, the U.S. FDA indicated that it would reconsider marijuana’s status as a Schedule I Controlled Substance. Legalization efforts have also gained ground in many U.S. states, with Oregon and Alaska becoming two battlegrounds for recreational legalization efforts over the coming year.
What’s New?
– Cannabis Therapy Hemp Farm Measures Up – Cannabis Therapy Corp.’s CTCO -1.00{92d3d6fd85a76c012ea375328005e518e768e12ace6b1722b71965c2a02ea7ce} initial hemp cultivars are already well underway measuring in at 16 inches high with normal healthy growth characteristics.
– Cannabis Cultivation Strains Energy Grid – Cannabis cultivation could be putting a strain on the nation’s energy grid, leading some regulators and companies to come up with innovative solutions to the problem.
– A Junior GW Play in the Cannabis Industry – CannabisFN takes a closer look at Cannabis Technologies Inc. CANLF -1.82{92d3d6fd85a76c012ea375328005e518e768e12ace6b1722b71965c2a02ea7ce} (cse:CAN), which is being billed by many as a junior GW Pharmaceutials in the making.
– Debunking the Cannabis-Schizophrenia Link – Cannabis critics face a new argument that there may be a reverse association where schizophrenia may cause cannabis use rather than the other way around.
– Cannabis Tech to Begin Phase I Glaucoma Trials – Cannabis Technologies Inc. CANLF -1.82{92d3d6fd85a76c012ea375328005e518e768e12ace6b1722b71965c2a02ea7ce} (cse:CAN) announced the start of Phase I clinical trials of its CTI-085 topical cannabinoid therapy for the treatment of glaucoma.
– Abattis Secures Key International Patent – Abattis Bioceuticals Corp. ATTBF -5.21{92d3d6fd85a76c012ea375328005e518e768e12ace6b1722b71965c2a02ea7ce} recently secured an International Patent for refining the optimal natural sources of nitric oxide in the human body.
Exclusive Interview Series
In a recent episode of CannabisFN’s Executive Interview Series, Mike Elliott sits down to talk with Cannabis Technologies Inc. CEO Craig Schneider to discuss the company’s Cannabinoid Drug Design Platform and its plans to develop treatments to specific medical conditions utilizing cannabinoids.
Click Here: Watch the Full Interview
What to Watch This Week
The cannabis sector as a whole moved slightly lower last week, but a number of public companies in the space jumped higher. Traders and investors will continue to watch for positive regulatory developments, particularly as the FDA appears ready to review marijuana’s status as a Schedule I Controlled Substance. The removal of that marker could open up the door to new opportunities in the space.
Upcoming Events
– WeedStock Conference – June 29 to July 1, 2014 – The 1st Annual Cannabis Investor Conference in Denver, Colorado will feature networking events, industry speakers, expert panels, and more.
About CannabisFN
CannabisFN.com is a dedicated financial network covering new, emerging and established companies operating in the burgeoning multi-billion dollar medical marijuana (“MMJ”) and cannabis industries. CannabisFN’s coverage is syndicated on the leading industry specific and mainstream financial websites and social media. To learn more and request a media kit, visit http://www.cannabisfn.com/market-defining-companies-program/ .
To subscribe to the CannabisFN newsletter or read additional coverage on cannabis laws and investments, visit http://www.cannabisfn.com .
Disclaimer: Except for the historical information presented herein, matters discussed in this article contain forward-looking statements that are subject to certain risks and uncertainties that could cause actual results to differ materially from any future results, performance or achievements expressed or implied by such statements. Emerging Growth LLC dba TDM Financial, which owns CannabisFN, is not registered with any financial or securities regulatory authority, and does not provide nor claims to provide investment advice or recommendations to readers of this release. Emerging Growth LLC dba TDM Financial, which owns CannabisFN, may from time to time have a position in the securities mentioned herein and may increase or decrease such positions without notice. For making specific investment decisions, readers should seek their own advice. Emerging Growth LLC dba TDM Financial, which owns CannabisFN, may be compensated for its services in the form of cash-based compensation or equity securities in the companies it writes about, or a combination of the two. For full disclosure please visit: http://www.cannabisfn.com/legal-disclaimer/ .
SOURCE: Emerging Growth LLC
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Copyright 2014 ACCESSWIRE
- Published in Medical Marijuana
Cannabis and Cannabinoids
Cannabinoids are a group of 21-carbon–containing terpenophenolic compounds produced uniquely by Cannabis species (e.g., Cannabis sativa L.) .[1,2] These plant-derived compounds may be referred to as phytocannabinoids. Although delta-9-tetrahydrocannabinol (THC) is the primary psychoactive ingredient, other known compounds with biologic activity are cannabinol, cannabidiol (CBD), cannabichromene, cannabigerol, tetrahydrocannabivarin, and delta-8-THC. CBD, in particular, is thought to have significant analgesic and anti-inflammatory activity without the psychoactive effect (high) of delta-9-THC.
One study in mice and rats suggested that cannabinoids may have a protective effect against the development of certain types of tumors.[3] During this 2-year study, groups of mice and rats were given various doses of THC by gavage. A dose-related decrease in the incidence of hepatic adenoma tumors and hepatocellular carcinoma (HCC) was observed in the mice. Decreased incidences of benign tumors (polyps and adenomas) in other organs (mammary gland, uterus, pituitary, testis, and pancreas) were also noted in the rats. In another study, delta-9-THC, delta-8-THC, and cannabinol were found to inhibit the growth of Lewis lung adenocarcinoma cells in vitro and in vivo .[4] In addition, other tumors have been shown to be sensitive to cannabinoid-induced growth inhibition.[5–8]
Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis invasion and metastasis.[9–12] Two reviews summarize the molecular mechanisms of action of cannabinoids as antitumor agents.[13,14] Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. These compounds have been shown to induce apoptosis in glioma cells in culture and induce regression of glioma tumors in mice and rats. Cannabinoids protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor.[15]
The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in HCC.[16] Both agents reduced the viability of HCC cells in vitro and demonstrated antitumor effects in HCC subcutaneous xenografts in nude mice. The investigations documented that the anti-HCC effects are mediated by way of the CB2 receptor. Similar to findings in glioma cells, the cannabinoids were shown to trigger cell death through stimulation of an endoplasmic reticulum stress pathway that activates autophagy and promotes apoptosis. Other investigations have confirmed that CB1 and CB2 receptors may be potential targets in non-small cell lung carcinoma [17] and breast cancer.[18]
An in vitro study of the effect of CBD on programmed cell death in breast cancer cell lines found that CBD induced programmed cell death, independent of the CB1, CB2, or vanilloid receptors. CBD inhibited the survival of both estrogen receptor–positive and estrogen receptor–negative breast cancer cell lines, inducing apoptosis in a concentration-dependent manner while having little effect on nontumorigenic, mammary cells.[19]
CBD has also been demonstrated to exert a chemopreventive effect in a mouse model of colon cancer.[20] In the experimental system, azoxymethane increased premalignant and malignant lesions in the mouse colon. Animals treated with azoxymethane and CBD concurrently were protected from developing premalignant and malignant lesions. In in vitro experiments involving colorectal cancer cell lines, the investigators found that CBD protected DNA from oxidative damage, increased endocannabinoid levels, and reduced cell proliferation. In a subsequent study, the investigators found that the antiproliferative effect of CBD was counteracted by selective CB1 but not CB2 receptor antagonists, suggesting an involvement of CB1 receptors.[21]
Another investigation into the antitumor effects of CBD examined the role of intercellular adhesion molecule-1 (ICAM-1).[12] ICAM-1 expression has been reported to be negatively correlated with cancer metastasis. In lung cancer cell lines, CBD upregulated ICAM-1, leading to decreased cancer cell invasiveness.
In an in vivo model using severe combined immunodeficient mice, subcutaneous tumors were generated by inoculating the animals with cells from human non-small cell lung carcinoma cell lines.[22] Tumor growth was inhibited by 60{92d3d6fd85a76c012ea375328005e518e768e12ace6b1722b71965c2a02ea7ce} in THC-treated mice compared with vehicle-treated control mice. Tumor specimens revealed that THC had antiangiogenic and antiproliferative effects. However, research with immunocompetent murine tumor models has demonstrated immunosuppression and enhanced tumor growth in mice treated with THC.[23,24]
In addition, both plant-derived and endogenous cannabinoids have been studied for anti-inflammatory effects. A mouse study demonstrated that endogenous cannabinoid system signaling is likely to provide intrinsic protection against colonic inflammation.[25] As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the risk reduction and treatment of colorectal cancer has been developed.[26–29]
CBD may also enhance uptake of cytotoxic drugs into malignant cells. Activation of the transient receptor potential vanilloid type 2 (TRPV2) has been shown to inhibit proliferation of human glioblastoma multiforme cells and overcome resistance to the chemotherapy agent carmustine.[30] In an in vitro model, CBD increased TRPV2 activation and increased uptake of cytotoxic drugs, leading to apoptosis of glioma cells without affecting normal human astrocytes. This suggests that coadministration of CBD with cytotoxic agents may increase drug uptake and potentiate cell death in human glioma cells.
Many animal studies have previously demonstrated that delta-9-THC and other cannabinoids have a stimulatory effect on appetite and increase food intake. It is believed that the endogenous cannabinoid system may serve as a regulator of feeding behavior. The endogenous cannabinoid anandamide potently enhances appetite in mice.[31] Moreover, CB1 receptors in the hypothalamus may be involved in the motivational or reward aspects of eating.[32]
Understanding the mechanism of cannabinoid-induced analgesia has been increased through the study of cannabinoid receptors, endocannabinoids, and synthetic agonists and antagonists. The CB1 receptor is found in both the central nervous system (CNS) and in peripheral nerve terminals. Similar to opioid receptors, increased levels of the CB1 receptor are found in regions of the brain that regulate nociceptive processing.[33] CB2 receptors, located predominantly in peripheral tissue, exist at very low levels in the CNS. With the development of receptor-specific antagonists, additional information about the roles of the receptors and endogenous cannabinoids in the modulation of pain has been obtained.[34,35]
Cannabinoids may also contribute to pain modulation through an anti-inflammatory mechanism; a CB2 effect with cannabinoids acting on mast cell receptors to attenuate the release of inflammatory agents, such as histamine and serotonin, and on keratinocytes to enhance the release of analgesic opioids has been described.[36–38] One study reported that the efficacy of synthetic CB1- and CB2-receptor agonists were comparable with the efficacy of morphine in a murine model of tumor pain.[39]
- Adams IB, Martin BR: Cannabis: pharmacology and toxicology in animals and humans. Addiction 91 (11): 1585-614, 1996. [PUBMED Abstract]
- Grotenhermen F, Russo E, eds.: Cannabis and Cannabinoids: Pharmacology, Toxicology, and Therapeutic Potential. Binghamton, NY: The Haworth Press, 2002.
- National Toxicology Program: NTP toxicology and carcinogenesis studies of 1-trans-delta(9)-tetrahydrocannabinol (CAS No. 1972-08-3) in F344 rats and B6C3F1 mice (gavage studies). Natl Toxicol Program Tech Rep Ser 446 (): 1-317, 1996. [PUBMED Abstract]
- Bifulco M, Laezza C, Pisanti S, et al.: Cannabinoids and cancer: pros and cons of an antitumour strategy. Br J Pharmacol 148 (2): 123-35, 2006. [PUBMED Abstract]
- Sánchez C, de Ceballos ML, Gomez del Pulgar T, et al.: Inhibition of glioma growth in vivo by selective activation of the CB(2) cannabinoid receptor. Cancer Res 61 (15): 5784-9, 2001. [PUBMED Abstract]
- McKallip RJ, Lombard C, Fisher M, et al.: Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease. Blood 100 (2): 627-34, 2002. [PUBMED Abstract]
- Casanova ML, Blázquez C, Martínez-Palacio J, et al.: Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. J Clin Invest 111 (1): 43-50, 2003. [PUBMED Abstract]
- Blázquez C, González-Feria L, Alvarez L, et al.: Cannabinoids inhibit the vascular endothelial growth factor pathway in gliomas. Cancer Res 64 (16): 5617-23, 2004. [PUBMED Abstract]
- Guzmán M: Cannabinoids: potential anticancer agents. Nat Rev Cancer 3 (10): 745-55, 2003. [PUBMED Abstract]
- Blázquez C, Casanova ML, Planas A, et al.: Inhibition of tumor angiogenesis by cannabinoids. FASEB J 17 (3): 529-31, 2003. [PUBMED Abstract]
- Vaccani A, Massi P, Colombo A, et al.: Cannabidiol inhibits human glioma cell migration through a cannabinoid receptor-independent mechanism. Br J Pharmacol 144 (8): 1032-6, 2005. [PUBMED Abstract]
- Ramer R, Bublitz K, Freimuth N, et al.: Cannabidiol inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1. FASEB J 26 (4): 1535-48, 2012. [PUBMED Abstract]
- Velasco G, Sánchez C, Guzmán M: Towards the use of cannabinoids as antitumour agents. Nat Rev Cancer 12 (6): 436-44, 2012. [PUBMED Abstract]
- Cridge BJ, Rosengren RJ: Critical appraisal of the potential use of cannabinoids in cancer management. Cancer Manag Res 5: 301-13, 2013. [PUBMED Abstract]
- Torres S, Lorente M, Rodríguez-Fornés F, et al.: A combined preclinical therapy of cannabinoids and temozolomide against glioma. Mol Cancer Ther 10 (1): 90-103, 2011. [PUBMED Abstract]
- Vara D, Salazar M, Olea-Herrero N, et al.: Anti-tumoral action of cannabinoids on hepatocellular carcinoma: role of AMPK-dependent activation of autophagy. Cell Death Differ 18 (7): 1099-111, 2011. [PUBMED Abstract]
- Preet A, Qamri Z, Nasser MW, et al.: Cannabinoid receptors, CB1 and CB2, as novel targets for inhibition of non-small cell lung cancer growth and metastasis. Cancer Prev Res (Phila) 4 (1): 65-75, 2011. [PUBMED Abstract]
- Nasser MW, Qamri Z, Deol YS, et al.: Crosstalk between chemokine receptor CXCR4 and cannabinoid receptor CB2 in modulating breast cancer growth and invasion. PLoS One 6 (9): e23901, 2011. [PUBMED Abstract]
- Shrivastava A, Kuzontkoski PM, Groopman JE, et al.: Cannabidiol induces programmed cell death in breast cancer cells by coordinating the cross-talk between apoptosis and autophagy. Mol Cancer Ther 10 (7): 1161-72, 2011. [PUBMED Abstract]
- Aviello G, Romano B, Borrelli F, et al.: Chemopreventive effect of the non-psychotropic phytocannabinoid cannabidiol on experimental colon cancer. J Mol Med (Berl) 90 (8): 925-34, 2012. [PUBMED Abstract]
- Romano B, Borrelli F, Pagano E, et al.: Inhibition of colon carcinogenesis by a standardized Cannabis sativa extract with high content of cannabidiol. Phytomedicine 21 (5): 631-9, 2014. [PUBMED Abstract]
- Preet A, Ganju RK, Groopman JE: Delta9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo. Oncogene 27 (3): 339-46, 2008. [PUBMED Abstract]
- Zhu LX, Sharma S, Stolina M, et al.: Delta-9-tetrahydrocannabinol inhibits antitumor immunity by a CB2 receptor-mediated, cytokine-dependent pathway. J Immunol 165 (1): 373-80, 2000. [PUBMED Abstract]
- McKallip RJ, Nagarkatti M, Nagarkatti PS: Delta-9-tetrahydrocannabinol enhances breast cancer growth and metastasis by suppression of the antitumor immune response. J Immunol 174 (6): 3281-9, 2005. [PUBMED Abstract]
- Massa F, Marsicano G, Hermann H, et al.: The endogenous cannabinoid system protects against colonic inflammation. J Clin Invest 113 (8): 1202-9, 2004. [PUBMED Abstract]
- Patsos HA, Hicks DJ, Greenhough A, et al.: Cannabinoids and cancer: potential for colorectal cancer therapy. Biochem Soc Trans 33 (Pt 4): 712-4, 2005. [PUBMED Abstract]
- Liu WM, Fowler DW, Dalgleish AG: Cannabis-derived substances in cancer therapy–an emerging anti-inflammatory role for the cannabinoids. Curr Clin Pharmacol 5 (4): 281-7, 2010. [PUBMED Abstract]
- Malfitano AM, Ciaglia E, Gangemi G, et al.: Update on the endocannabinoid system as an anticancer target. Expert Opin Ther Targets 15 (3): 297-308, 2011. [PUBMED Abstract]
- Sarfaraz S, Adhami VM, Syed DN, et al.: Cannabinoids for cancer treatment: progress and promise. Cancer Res 68 (2): 339-42, 2008. [PUBMED Abstract]
- Nabissi M, Morelli MB, Santoni M, et al.: Triggering of the TRPV2 channel by cannabidiol sensitizes glioblastoma cells to cytotoxic chemotherapeutic agents. Carcinogenesis 34 (1): 48-57, 2013. [PUBMED Abstract]
- Mechoulam R, Berry EM, Avraham Y, et al.: Endocannabinoids, feeding and suckling–from our perspective. Int J Obes (Lond) 30 (Suppl 1): S24-8, 2006. [PUBMED Abstract]
- Fride E, Bregman T, Kirkham TC: Endocannabinoids and food intake: newborn suckling and appetite regulation in adulthood. Exp Biol Med (Maywood) 230 (4): 225-34, 2005. [PUBMED Abstract]
- Walker JM, Hohmann AG, Martin WJ, et al.: The neurobiology of cannabinoid analgesia. Life Sci 65 (6-7): 665-73, 1999. [PUBMED Abstract]
- Meng ID, Manning BH, Martin WJ, et al.: An analgesia circuit activated by cannabinoids. Nature 395 (6700): 381-3, 1998. [PUBMED Abstract]
- Walker JM, Huang SM, Strangman NM, et al.: Pain modulation by release of the endogenous cannabinoid anandamide. Proc Natl Acad Sci U S A 96 (21): 12198-203, 1999. [PUBMED Abstract]
- Facci L, Dal Toso R, Romanello S, et al.: Mast cells express a peripheral cannabinoid receptor with differential sensitivity to anandamide and palmitoylethanolamide. Proc Natl Acad Sci U S A 92 (8): 3376-80, 1995. [PUBMED Abstract]
- Ibrahim MM, Porreca F, Lai J, et al.: CB2 cannabinoid receptor activation produces antinociception by stimulating peripheral release of endogenous opioids. Proc Natl Acad Sci U S A 102 (8): 3093-8, 2005. [PUBMED Abstract]
- Richardson JD, Kilo S, Hargreaves KM: Cannabinoids reduce hyperalgesia and inflammation via interaction with peripheral CB1 receptors. Pain 75 (1): 111-9, 1998. [PUBMED Abstract]
- Khasabova IA, Gielissen J, Chandiramani A, et al.: CB1 and CB2 receptor agonists promote analgesia through synergy in a murine model of tumor pain. Behav Pharmacol 22 (5-6): 607-16, 2011. [PUBMED Abstract]
- Published in Blog
Highmark Enters Into a Binding Letter of Intent to Acquire BCBUD Producers Inc.
Highmark Marketing Inc. (CSE:HMK) (“Highmark”) is pleased to announce that it has entered into a binding letter of intent (the “Letter”) with BCBUD Producers Inc. (“BCBUD”) to acquire 100{92d3d6fd85a76c012ea375328005e518e768e12ace6b1722b71965c2a02ea7ce} of the authorized share capital of BCBUD (the “Acquisition”) from BCBUD’s shareholder, Blue Moon Advertising Inc. (“Blue Moon”).
BCBUD has prepared an application to become a licensed producer (“LP”) of marijuana and has informed Highmark that it is ready to file the application (the “Application”) under the Marijuana for Medical Purposes Regulations (“MMPR”). Highmark will cover BCBUD’s business costs relating to the Application up to a maximum of $100,000.
Highmark Marketing Inc. (CSE:HMK) (“Highmark”) is pleased to announce that it has entered into a binding letter of intent (the “Letter”) with BCBUD Producers Inc. (“BCBUD”) to acquire 100{92d3d6fd85a76c012ea375328005e518e768e12ace6b1722b71965c2a02ea7ce} of the authorized share capital of BCBUD (the “Acquisition”) from BCBUD’s shareholder, Blue Moon Advertising Inc. (“Blue Moon”).
BCBUD has prepared an application to become a licensed producer (“LP”) of marijuana and has informed Highmark that it is ready to file the application (the “Application”) under the Marijuana for Medical Purposes Regulations (“MMPR”). Highmark will cover BCBUD’s business costs relating to the Application up to a maximum of $100,000.
BCBUD has an option to lease a 27,000 square foot building in the Township of Langley, British Columbia. The property is zoned M-2, and when the facility is operational it could be capable of producing up to 2,000,000 grams (4409 pounds) of medical marijuana per year with the additional possibility of expansion adjacent to the site.
BCBUD cannot legally become a producer under the MMPR Act until it has been granted a license, and it is currently not known if and when BCBUD will obtain that license. The key milestones to obtaining a LP license include filing an application, receiving a “Ready to Build” notice, completion of the upgrades as per the application, approval to produce upon inspection of the facility, and finally approval to distribute the product to patients. Bill Marshall, President of BCBUD, has gained extensive experience with MMPR applications while working with one of the most prolific consultants to prospective licensed producers. As the Senior Person in Charge he will be responsible for advancing the application in a timely fashion, and will have the support of the Highmark team during this process. Highmark has agreed to issue 250,000 Common Shares of Highmark to Blue Moon at the time the Application has been filed by BCBUD with Health Canada.
Once the “Ready-to-Build” notice has been received from Health Canada, Highmark will have 3 months to complete the Acquisition by issuing 2,250,000 Common Shares of Highmark to Blue Moon (the “Acquisition Shares”). If Highmark completes the Acquisition, it has committed to funding another $1,500,000 for upgrading the security, electrical, plumbing, ventilation and other improvements as per the application. At the point of receiving the “Ready to Build” notice Highmark intends to seek an equity financing in the amount of $1,500,000 to meet its obligations. In the event that a license to produce marijuana is not received within 18 months, the Acquisition Shares may be subject to cancelation.
About Highmark
Highmark is a nutraceutical company, based in British Columbia, focused on bringing the health benefits of natural and herbal remedies to the market. Highmark intends to acquire, license, distribute, and market products in the nutraceutical industry.
Further information about Highmark is available under its profile on the SEDAR websitewww.sedar.com and on Highmark’s page on the CSE website.
The CSE has not reviewed, nor approved or disapproved the content of this press release.
Forward-Looking Information:
This press release may include forward-looking information within the meaning of Canadian securities legislation, concerning the business of Highmark. Forward-looking information is based on certain key expectations and assumptions made by the management of Highmark, including future plans for acquisitions. Although Highmark believes that the expectations and assumptions on which such forward-looking information is based are reasonable, undue reliance should not be placed on the forward-looking information because Highmark can give no assurance that they will prove to be correct. Forward-looking statements contained in this press release are made as of the date of this press release. Highmark disclaims any intent or obligation to update publicly any forward-looking information, whether as a result of new information, future events or results or otherwise, other than as required by applicable securities laws.
This news release does not constitute an offer to sell or a solicitation of an offer to buy any of the securities described herein in the United States. The securities described herein have not been and will not be registered under the United States Securities Act of 1933, as amended, or any applicable securities laws or any state of the United States and may not be offered or sold in the United States or to the account or benefit of a person in the United States absent an exemption from the registration requirements.
Highmark Marketing Inc.
Marc Branson
Chief Executive Officer
604.283.1722
info@highmarkcorp.ca
- Published in Medical Marijuana