Sativa Science makes no therapeutic claims about any of our products. All of the listed products are classified by the FDA as supplements. We believe any recommendations regarding the use of these products for health reasons should come from a health care provider. Don’t have one? See our list of providers with expertise in Cannabis.

Why believe we have the best medical grade products on the medical Cannabis market. This is because we concentrate on only a few of the most clinically useful molecules. We have focused our development on sound pharmacologic principles. 

Purity:  Our cannabis gel caps contain only high grade hemp extracts sourced from reputable growers with contaminant testing of the raw hemp prior to processing, and again after processing into isolates. The cannabinoids in our products are extracted with advanced methods, which require no harsh solvents. Our products are cGMP certified demonstrating they are produced in accordance with Good Manufacturing Practices and our facilities are ISO certified ensuring we consistently exceed the highest regulatory requirements of quality, consistency, and safety. Each batch of final product is tested for cannabinoid purity by Sativa Science in an independent laboratory and is guaranteed to be pure. We meet current FDA standards for purity and potency.

Bioavailability: To maximize bioavailability, these highly purifed isolates are homogenized with extra virgin (unprocessed) olive oil, a long chain triglyceride (LCT). Using olive oil as the carrier results in 3-4 times greater lymphatic absorption versus medium chain triglycerides. This means less of the molecule is being metabolized by the liver, thus higher serum concentrations.

Easy Oral Dosing: Our softgels are dosed once or twice daily in strengths that make sense

High Patient Compliance: Our vegan softgels are made from plant derived materials (cassava root extract), and come in induction sealed bottles. Our 0.5 ml softgels are small, easy to swallow, and shipped directly to your patients home.

Reproducible Potency: means no variability month to month

Robust Supply Chain: This means you are assured of continued access to products that work.

Affordable: We work hard to keep our products affordable to patients. We have the lowest cost molecules available.

Our Current Product Line

Cannabigerol (CBG) 100 mg

Pharmacodynamics (how CBG affects the body):  CBG binds to several cellular target proteins. It is a weak partial agonist at CB1 and CB2 receptors. CBG Is a 5-HT1A (50 nM affinity) and 5HT2A receptor antagonist (unlike CBD which is an indirect agonist at 5-HT1A). CBG is a potent alpha 2 adrenergic receptor agonist, with sub-nanomolar affinity. CBG is an agonist at the gamma peroxisome proliferator-activated receptor (PPAR). This nuclear receptor forms a heterodimer which binds directly to DNA and functions as a transcription factor to regulate the expression of genes involved in lipid and hepatic metabolism and inflammation. CBG binds to a number of the transient receptor potential (TRP) receptors: TRPA1 (agonist), TRPV1 (unknown), TRPV2 (agonist) TRPV3 (agonist), TRPV4 (agonist), and TRPM8 (antagonist). These receptors are widely distributed in many tissues, including central and peripheral neurons and are involved in a number of processes including nociception and programmed (apoptotic) cell death. CBG inhibits the reuptake of endocannabinoids, potentiating their action.

Pharmacokinetics (how the body affects CBG): CBG is a small lipophilic molecule that accumulates in fatty tissues and penetrates highly into adipose tissue, brain, heart, liver, lung, and spleen. It is metabolized by the cytochrome p450 enzymes CYP2J2, CYP3A4, CYP2D6, CYP2C8, and CYP2C9. CBG inhibits CYP2D6 and CYP3A4CBG. CBG is metabolized by (is a substrate of) CYP3A4, CYP2J2, CYP2D6, CYP2C8, and CYP2C9. CBG is not known to be an inducer. The major metabolite of CBG is cyclo-CBG. CBG is rapidly absorbed after oral administration, is bioactive, peaks in the brain in 120 minutes, and has a serum elimination half-life of 2-6 hours.

Cannabinol (CBN) 30 mg

Pharmacodynamics (how CBN affects the body):  CBN is an agonist at CB1 and CB2 receptors. With some evidence of slightly higher affinity at CB2 (Ki 126 nM). CBN is a low affinity agonist at the transient receptor potential receptors TRPV1, TRPV2, TRPV3, TRPV4, and TRPA1, and an antagonist at TRPM8. CBN inhibits interleukin synthesis. Strong inhibitor of methicillin-resistant staphylococcus aureus (MRSA) production.

Pharmacokinetics (how the body affects CBN): C BN is a small lipophilic molecule that accumulates in fatty tissues and penetrates highly into adipose tissue, brain, heart, liver, lung, and spleen. It has low oral absorption (<10%). CBN is metabolized by (is a substrate of) CYP3A4, CYP2C9, UGT1A7, UGT1A8, UGT1A9, UGT1A10, UGT2B7. CBN inhibits CYP2B6, CYP2C9, CYP2E1, CYP1B1, CYP1A2, CYP1B1, UGT1A9. CBN induces UGT2B7. The first pass active metabolite through hydroxylation, 11-OH-CBN, is 2x as potent as CBN.

Cannabichromene (CBC) 50 mg

Pharmacodynamics (how CBN affects the body):  CBC has multiple mechanisms of action. It modulates endocannabinoid tone through inhibition of monoacylglycerol lipase and blocking the reuptake of the endocannabinoids N-arachidonoylethanolamine (AEA or anandamide) and 2-arachidonoylglycerol (2-AG). CBC binds weakly to CB1 and CB2 receptors with binding affinities of 713 nM and 256 nM, respectively, and acts as a CB2 agonist, stimulating cAMP production and modulating inflammation. CBC acts on several transient receptor potential channels: TRPV (unknown), TRPV3 (agonist), TRPV4 (agonist), and TRPA1 (activator and desensitizer). It is also a low-potency antagonist at TRPM8 receptors. CBC is an antagonist of beta-arrestin, a protein that regulates G-protein-coupled receptor (GPCR) desensitization, signaling, and internalization. CBC binds to peroxisome proliferator-activated receptors (PPARs), nuclear proteins that act as transcription factors, regulating the expression of genes involved in lipid and hepatic metabolism and inflammation.

Pharmacokinetics (how the body affects CBC):  CBC is a small lipophilic molecule that accumulates in fatty tissues and penetrates highly into adipose tissue, brain, heart, liver, lung, and spleen. It has low oral absorption, around 10%. It is >90% protein bound. CBC plasma levels peak in 2.3-4.3 hours after an oral dose. There is a dose-dependent increase in steady state plasma levels.

Cannabidiol (CBD) 75 mg and 150 mg

Pharmacodynamics (how CBD affects the body):  CBD has multiple demonstrated mechanisms of action. It binds with low affinity to and acts as a noncompetitive antagonist at both CB1 and CB2 receptors, and an inverse agonist at the CB2 receptor, making it a negative allosteric modulator and not a primary ligand at either receptor. CBD inhibits fatty acid aminohydrolase (FAAH), an enzyme that breaks down endocannabinoids and inhibits the reuptake of anandamide, potentiating endocannabinoid signaling. CBD is a GPR55 antagonist and a T calcium channel blocker, with an IC50 of 1 micromolar, supporting a role in intracellular calcium regulation. GPR55 receptors are enriched in the dorsal root ganglia, critical to central pain modulation. CBD acts as an agonist and positive allosteric modulator at the 5HT1a receptor, which plays a critical role in the pathways mediating aggression, depression, and anxiety. A significant effect of CBD is through inhibition of the bi-directional nucleoside transporter, at an IC50 of 120 nM, potentiating adenosine action. CBD interacts with 6 transient receptor potential channels activating TRPV1, TRPV2, TRPV3, TRPV4, and TRPA1 and antagonizing TRPM8 and A2 adrenoceptors. These channels are present in a variety of cell types including neurons and are involved in both central and peripheral pathways modulating visceral, neuropathic, and inflammatory pain. CBD is also a positive allosteric modulator at the GABA A α1-6βγ2 receptor, with low micromolar potencies. CBD exerts anti-inflammatory and antioxidant effects through interactions with the interferon beta (IFN-B) and nuclear factor-kappa B (NF-κB) pathways. CBD inhibits chemotactic mediators involved in neutrophil activation, affects the humoral immune response by suppressing T cells, and downregulates pro-inflammatory and profibrotic cytokines. CBD can downregulate the mammalian target of rapamycin (mTOR) receptors, which regulate cell proliferation and apoptosis and can induce apoptosis in several cancer cell lines including breast carcinoma, glioma, leukemia, thymoma, neuroblastoma, prostate, and colon cancers. CBD is a nonselective voltage-gated sodium channel blocker and blocks potassium channel delayed rectifier currents.

Pharmacokinetics (how the body affects CBD): CBD is a small lipophilic molecule that accumulates in fatty tissues and penetrates highly into adipose tissue, brain, heart, liver, lung, and spleen. It has low oral absorption (<10%). Its mean half-life is about 24 hours after oral ingestion. It is >95% protein bound. CBD is extensively metabolized in the liver, and excreted in the stool and, to a lesser extent, in the urine. CBD is metabolized (is a substrate of) the hepatic P450 enzymes CYP3A4, CYP2C19, CYP1A1,UGT1A7, UGT1A9, and UGT2B7. CBD inhibits CYP2C9, CYP2C19, CYP2D6, CYP2C8, CYP1A2, CYP3A4, CYP1B1, CYP2B6, UGT1A9, UGT2B7, P-gp, and CES1 (carboxylesterase 1). CBD induces CYP2B6. CBD may lower the serum levels of clobazam, rufinamide, and valproic acid. Its action on CBD CYP2C19 may increase serum levels of N-desmethyl clobazam. Strong inducers of CYP3A4 and CYP2C19 may affect CBD exposure. CBD may affect exposure to CYP2C19 substrates (eg, clobazam, diazepam, stiripentol), orally administered P-gp substrates, or other substrates. 7-OH-CBD is an active metabolite. Consider dose reduction of orally administered everolimus, with appropriate therapeutic drug monitoring, when everolimus is combined with CBD. Concomitant use of CBD and valproate increases the incidence of liver enzyme elevations.

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