hTRPV1 (EC50 = 290 nM, HEK293 cells)[1]

In a dose- and time-dependent way, capsaicin (50–300 µM; 24-72 hours) significantly inhibited cell proliferation. It is estimated that the IC50 value is 150 µM[2]. Over a 24-72-hour period, capsaicin (50-300 µM) increases the expression of pro-apoptotic Bad/Bax and decreases anti-apoptotic Bcl-2 protein. It also activates caspase 3 and PARP (p85) levels in the cytosol[2]. Sub-G1 DNA concentration, nuclear condensation, and nuclear DNA fragmentation are all increased by capsaicin [2]. By downregulating the production of cyclin B1 and D1 regulatory factors as well as cyclin-dependent protein kinases cdk-1, cdk-2, and cdk-4, capsaicin prevents cell cycle progression in the G1/S phase in FaDu cells [2].

By altering the protein expression of the apoptotic regulatory factors p53, Bcl-2, Bax, and caspase-3, capsaicin prevents the growth of lung cancer [2].

Cloning and expression of human TRPV1[1]
A human embryonic kidney cell line stably expressing human TRPV1 (hTRPV1.HEK293 cells) was generated as described previously (Hayes et al., 2000). Cells were cultured on plastic tissue culture dishes in modified Eagles's medium with Earle's salts and supplemented with 10% fetal bovine serum, nonessential amino acids and 0.2 mm l-glutamine while being maintained under 5% CO2 at 37°C. For electrophysiological experiments, cells were plated at a 30,000 cells cm−2 density onto 19 mm glass coverslips coated with poly-l-lysine with experiments being performed 24–48 h thereafter.[1]

---

Electrophysiological techniques[1]
Whole-cell patch-clamp experiments were performed according to standard methods, using an Axopatch 200B amplifier, as described previously (Hayes et al., 2000). Thick-walled borosilicate glass electrodes having 1.5–4 mΩ resistance were used to record currents following drug application using an automated three-barrelled solution switching device. The extracellular solution consisted of (mm): NaCl, 130; KCl, 5; BaCl2, 2; MgCl2, 1; glucose, 30; HEPES-NaOH, 25; pH 7.3 and electrodes were filled with intracellular solution as follows (mm): CsCl, 140; MgCl2, 4; EGTA, 10; HEPES-CsOH, 10; pH 7.3. Concentration–response curves were generated by comparing the peak response evoked by a test concentration of agonist to that evoked by a previous control current recorded in response to 1 μm capsaicin. Current–voltage relationships were established by measuring the net agonist-evoked current response during a voltage ramp (−70 to +70 mV). A baseline, obtained from the mean of two or three voltage-ramps in control solution prior to drug addition, was subtracted from the mean of three to five voltage-ramps at peak current in presence of drug (see Figure 2c). In these experiments, all data were normalised to the initial current obtained at the holding potential of −70 mV.

Cell Viability Assay[2]
Cell Types: Human Pharyngeal Squamous Carcinoma Cells (FaDu)
Tested Concentrations: 50 µM, 100 µM, 200 µM and 300 µM
Incubation Duration: 24 hrs (hours), 48 hrs (hours) and 72 hrs (hours)
Experimental Results: Cell growth shown.

---

Apoptosis analysis[2]
Cell Types: FaDu Cell
Tested Concentrations: 50 µM, 100 µM and 200 µM
Incubation Duration: 12 hrs (hours)
Experimental Results: The activity of caspase 3 increased in a time-dependent manner.

---

Western Blot Analysis[2]
Cell Types: FaDu Cell
Tested Concentrations: 200 µM
Incubation Duration: 24 hrs (hours)
Experimental Results: Activation of caspase 3 and PARP (p85) levels was observed.

Animal/Disease Models: Benzo(a)pyrene-induced Swiss albino mice (20-25 g; 8-10 weeks old) [3]
Doses: 10 mg/kg
Route of Administration: intraperitonealadministration; intraperitonealadministration. Once a week for 14 consecutive weeks
Experimental Results: Inhibits the development of lung cancer in mice.

[1]. McNamara FN, et al. Effects of piperine, the pungent component of black pepper, at the human vanilloid receptor (TRPV1). Br J Pharmacol. 2005 Mar;144(6):781-90.
[2]. Shin YH, et al. The Effect of Capsaicin on Salivary Gland Dysfunction. Molecules. 2016 Jun 25;21(7).
[3]. Anandakumar P, et al. Capsaicin provokes apoptosis and restricts benzo(a)pyrene induced lung tumorigenesis in Swiss albino mice. Int Immunopharmacol. 2013 Jun 6;17(2):254-259.

Capsaicin is a capsaicinoid. It has a role as a non-narcotic analgesic, a voltage-gated sodium channel blocker and a TRPV1 agonist.
Capsaicin is most often used as a topical analgesic and exists in many formulations of cream, liquid, and patch preparations of various strengths; however, it may also be found in some dietary supplements. Capsaicin is a naturally-occurring botanical irritant in chili peppers, synthetically derived for pharmaceutical formulations. The most recent capsaicin FDA approval was Qutenza, an 8% capsaicin patch dermal-delivery system, indicated for neuropathic pain associated with post-herpetic neuralgia.
Capsaicin is a natural product found in Capsicum pubescens, Capsicum annuum, and Capsicum with data available.
Capsaicin is a chili pepper extract with analgesic properties. Capsaicin is a neuropeptide releasing agent selective for primary sensory peripheral neurons. Used topically, capsaicin aids in controlling peripheral nerve pain. This agent has been used experimentally to manipulate substance P and other tachykinins. In addition, capsaicin may be useful in controlling chemotherapy- and radiotherapy-induced mucositis.

---

Capsaicin is identified as the primary pungent principle in Capsicum fruits. Hot chili peppers that belong to the plant genus Capsicum (family Solanaceae) are among the most heavily consumed spices throughout the world. The capsaicin content of green and red peppers ranges from 0.1 to 1%. Capsaicin evokes numerous biological effects and thus has been the target of extensive., investigations since its initial identification in 1919. One of the most recognized physiological properties of capsaicin is its selective effects on the peripheral part of the sensory nervous system, particularly on the primary afferent neurons. The compound is known to deplete the neurotransmitter of painful impulses known as substance P from the sensory nerve terminals, which provides a rationale for its use as a versatile experimental tool for studying pain mechanisms and also for pharmacotherapy to treat some peripheral painful states, such as rheumatoid arthritis, post-herpetic neuralgia, post-mastectomy pain syndrome and diabetic neuropathy. Considering the frequent consumption of capsaicin as a food additive and its current therapeutic application, correct assessment of any harmful effects of this compound is important from the public health standpoint. Ingestion of large amounts of capsaicin has been reported to cause histopathological and biochemical changes, including erosion of gastric mucosa and hepatic necrosis. However, there are contradictory data on the mutagenicity of capsaicin. A recent epidemiological study conducted in Mexico revealed that consumers of chili pepper were at higher risk for gastric cancer than non-consumers. However, it remains unclear whether capsaicin present in hot chili pepper is a major causative factor in the aetiology of gastric cancer in humans. A growing number of recent studies have focused on anticarcinogenic or antimutagenic phytochemicals, particularly those included in human diet. In summary, capsaicin has dual effects on chemically induced carcinogenesis and mutagenesis. Although a minute amount of capsaicin displays few or no deleterious effects, heavy ingestion of the compound has been associated with necrosis, ulceration and even carcinogenesis. Capsaicin is considered to be metabolized by cytochrome P-450-dependent mixed-function oxidases to reactive species. (A7835). A7835: Surh YJ, Lee SS: Capsaicin in hot chili pepper: carcinogen, co-carcinogen or anticarcinogen? Food Chem Toxicol. 1996 Mar;34(3):313-6. PMID:8621114
An alkylamide found in CAPSICUM that acts at TRPV CATION CHANNELS.

C18H27NO3

293.4012

305.19909

C, 70.79; H, 8.91; N, 4.59; O, 15.72

404-86-4

Capsaicinoid;404-86-4;(E/Z)-Capsaicin-d3;1185237-43-7;(Z)-Capsaicin;25775-90-0;Capsaicin-d3;1217899-52-9

1548943

Typically exists as white to off-white solids at room temperature

1.0±0.1 g/cm3

469.7±55.0 °C at 760 mmHg

62-65 °C

237.9±31.5 °C

0.0±1.2 mmHg at 25°C

1.508

4.27

58.56

CC(C)/C=C/CCCCC(NCC1=CC=C(O)C(OC)=C1)=O

YKPUWZUDDOIDPM-SOFGYWHQSA-N

InChI=1S/C18H27NO3/c1-14(2)8-6-4-5-7-9-18(21)19-13-15-10-11-16(20)17(12-15)22-3/h6,8,10-12,14,20H,4-5,7,9,13H2,1-3H3,(H,19,21)/b8-6+

8-Methyl-N-vanillyl-(trans)-6-nonenamide

(E)-Capsaicin Capsicine Capsicin PS C (E)Capsaicin; Zostrix; CAPSAICINE; Qutenza; Styptysat; Axsain;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~327.43 mM)

Solubility in Formulation 1: ≥ 20 mg/mL (65.49 mM) (saturation unknown) in 10% EtOH + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 200.0 mg/mL clear EtOH stock solution to 900 μL of corn oil and mix evenly.

---

Solubility in Formulation 2: ≥ 2.5 mg/mL (8.19 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

---

View More

Solubility in Formulation 3: ≥ 2.5 mg/mL (8.19 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

---

Solubility in Formulation 4: ≥ 2.5 mg/mL (8.19 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL corn oil and mix evenly.

---

 (Please use freshly prepared in vivo formulations for optimal results.)