Ginsenoside Ro acts as a Ca2+-antagonist, which contributes to its antiplatelet effect. It reduces thrombin-stimulated platelet aggregation in a dose-dependent manner. It reduces the production of TXA2 more than it reduces the activities of COX-1 and TXA5. It also has anti-inflammatory activity.

The new and advantageous Ca2+ antagonist chemical ginsenoside Ro found in ginseng has the potential to prevent thrombotic disorders caused by platelet aggregation. Thrombin-stimulated platelet aggregation is dose-dependently inhibited by ginsenoside Ro, with an IC50 of about 155 μM [1]. Thrombin-induced platelet aggregation is prevented by ginsenoside Ro, which also suppresses the synthesis of TXA2. Platelet aggregation and thrombosis are facilitated by thromboxane A2 (TXA). Thrombin-induced TXB2 levels can be decreased dose-dependently (50-300 μM) by ginsenoside Ro; thrombin-mediated elevation of TXB2 levels can be inhibited by 94.9% at 300 μM. The protein COX-1 activity was 2.3 ± 0.1 nmol/mg when ginsenoside Ro (negative control) was depleted. The activity of COX-1 was, however, dose-dependently diminished by ginsenoside Ro (50–300 μM); at 300 μM, the activity of COX-1 was 26.4% lower than that of the negative control. The activity of TXA2 synthase (TXAS) was 220.8±1.8 ng/mg protein/min in the absence of ginsenoside Ro (negative control). In contrast, TXAS activity dropped by 22.9% at 300 μM relative to the negative control when ginsenoside Ro was added in a dose-dependent manner (50-300 μM). In comparison to its inhibitory effect on COX-1 (26.4%) and TXAS (22.9%) activities, ginsenoside Ro (300 μM) has a far greater effect on TXB2 production (94.9%) [2]. At 10 μM, 50 μM, 100 μM, and 200 μM concentrations, ginsenoside Ro was first treated for 24 hours in order to assess its toxicity in Raw 264.7 cells. No clear dose-dependent toxicity was observed in ginsenoside Ro. The impact of ginsenoside Ro on oxidative stress indicators (ROS) levels and cell viability were then assessed following an exposure to 1 μg/mL LPS. Approximately 70% less cells were viable after exposure to LPS than after no treatment. The viability of the cells was greatly increased by pretreating them with 100 μM and 200 μM ginsenoside Ro for one hour before incubating them with 1 μg/mL LPS for 24 hours. Ginsenoside Ro's effects on vitality are compatible with changes in ROS levels and NO generation [3].
In vitro, Ginsenoside Ro dose-dependently reduces thrombin-stimulated platelet aggregation, with an IC50 of approximately 155 μM. It exhibits a Ca2+-antagonistic effect, which is the basis for its antiplatelet activity. These effects have been demonstrated in platelet aggregation assays.

Prior to intravenous injection of HT29, mice were given water-soluble ginsenoside Ro by gavage at doses of 25 and 250 mg/kg/day for four days in order to maintain blood concentrations of ginsenoside Ro. The mice were then given ginsenoside Ro intravenously for 40 days after the level was reached. Following a 38-day course of therapy, the animals were slaughtered, and HT29 assessed the toxicity of ginsenoside Ro and mouse histology in addition to counting the number of lung metastases. With an 88% (P < 0.01) inhibition rate, ginsenoside Ro (250 mg/kg/day) can dramatically lower the amount of tumor nodules on the lung surface [4].
In vivo, Ginsenoside Ro inhibits an increase in vascular permeability in mice induced by acetic acid at doses of 10, 50, and 200 mg/kg (p.o.). This demonstrates its anti-inflammatory activity in an animal model. It also has anti-proliferative and anti-hepatitis activities.

In vitro enzyme/receptor binding assays for Ginsenoside Ro involve measuring its Ca2+-antagonistic activity. These assays typically use platelet preparations to assess its effects on calcium signaling and platelet aggregation. Its effects on COX-1 and TXA5 activities may also be studied using enzymatic assays.

In vitro cell-based assays for Ginsenoside Ro involve treating platelets to assess its effects on aggregation and calcium signaling. Its anti-inflammatory activity is evaluated using immune cells. Its anti-proliferative effects are studied in various cell lines.

In vivo animal experiments for Ginsenoside Ro have been conducted in mice to study its anti-inflammatory effects. The compound is administered orally, and its effect on vascular permeability induced by acetic acid is measured. Its anti-hepatitis activity has also been studied in animal models.

Ginsenoside Ro is soluble in water, methanol, and ethanol, but insoluble in chloroform, ether, and benzene. Its melting point is 239-241°C, and its specific rotation is [α]D +15.93° (c, 0.91 in MeOH). Specific pharmacokinetic data is not detailed.

Specific toxicity data for Ginsenoside Ro is not provided in the search results. As a component of Panax ginseng, it is generally considered safe. Its anti-inflammatory and antiplatelet activities suggest a potential protective role in cardiovascular diseases.

[1]. Inhibitory Effects of Cytosolic Ca2+ Concentration by Ginsenoside Ro Are Dependent on Phosphorylation of IP3RI and Dephosphorylation of ERK in Human Platelets. Evid Based Complement Alternat Med. 2015;2015:764906.

[2]. Inhibitory effects of thromboxane A2 generation by ginsenoside Ro due to attenuation of cytosolic phospholipase A2 phosphorylation and arachidonic acid release. J Ginseng Res. 9 Jan 2018.

[3]. Upregulation of heme oxygenase-1 by ginsenoside Ro attenuates lipopolysaccharide-induced inflammation in macrophage cells. J Ginseng Res. 2015 Oct;39(4):365-70.

[4]. The traditional Chinese medicine Achyranthes bidentata and our de novo conception of its metastatic chemoprevention: from phytochemistry to pharmacology. Sci Rep. 2017 Jun 20;7(1):3888.

Bamboo saponin V is a triterpenoid saponin with the function of a metabolite. Ginsenoside Ro has been reported in ginseng, Japanese ginseng, and other organisms with relevant data. See also: Asian ginseng (partial list).
Ginsenoside Ro is an oleanane-type saponin from Panax ginseng with antiplatelet, anti-inflammatory, and anti-hepatitis activities. It acts as a Ca2+-antagonist and reduces platelet aggregation. It is a research compound with potential therapeutic applications.

C48H76O19

957.12

956.498

34367-04-9

11815492

White to off-white solid powder

1.14

1018.6±65.0 °C at 760 mmHg

241 °C

289.2±27.8 °C

0.0±0.6 mmHg at 25°C

1.627

6.29

11

19

10

67

1880

23

C[C@]12CC[C@@H](C([C@@H]1CC[C@@]3([C@@H]2CC=C4[C@]3(CC[C@@]5([C@H]4CC(CC5)(C)C)C(=O)O[C@H]6[C@@H]([C@H]([C@@H]([C@H](O6)CO)O)O)O)C)C)(C)C)O[C@H]7[C@@H]([C@H]([C@@H]([C@H](O7)C(=O)O)O)O)O[C@H]8[C@@H]([C@H]([C@@H]([C@H](O8)CO)O)O)O

NFZYDZXHKFHPGA-QQHDHSITSA-N

InChI=1S/C48H76O19/c1-43(2)14-16-48(42(61)67-40-35(58)31(54)29(52)24(20-50)63-40)17-15-46(6)21(22(48)18-43)8-9-26-45(5)12-11-27(44(3,4)25(45)10-13-47(26,46)7)64-41-37(33(56)32(55)36(65-41)38(59)60)66-39-34(57)30(53)28(51)23(19-49)62-39/h8,22-37,39-41,49-58H,9-20H2,1-7H3,(H,59,60)/t22-,23+,24+,25-,26+,27-,28+,29+,30-,31-,32-,33-,34+,35+,36-,37+,39-,40-,41+,45-,46+,47+,48-/m0/s1

(2S,3S,4S,5R,6R)-6-[[(3S,4aR,6aR,6bS,8aS,12aS,14aR,14bR)-4,4,6a,6b,11,11,14b-heptamethyl-8a-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxycarbonyl-1,2,3,4a,5,6,7,8,9,10,12,12a,14,14a-tetradecahydropicen-3-yl]oxy]-3,4-dihydroxy-5-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyoxane-2-carboxylic acid

Chikusetsusaponin V; Chikusetsusaponin 5; Ginsenoside Ro

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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 (~104.48 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (2.61 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.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (2.61 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.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (2.61 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 of corn oil and mix evenly.

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