Product Information
Registration Status: ActiveSIN03486P
SANKAIJO TABLET is approved to be sold in Singapore with effective from 1989-06-24. It is marketed by SATO PHARMACEUTICAL (SINGAPORE) PTE LTD, with the registration number of SIN03486P.
This product contains Aloe 12.5mg,Rhubarb 25mg, and Senna 25mg in the form of TABLET, FILM-COATED. It is approved for ORAL use.
This product is manufactured by SATO PHARMACEUTICAL CO. in TAIWAN.
It is an Over-the-counter Medicine that can be freely obtained from any retailer
Product Reference
Important Note: For generic product, the SPC/PIL provided may not be brand specific.
{{/items}} {{^items}}Description
Aloe describes a genus including over 500 species of flowering succulent plants that grow in the Southern peninsula and various islands. Aloe vera, or _Aloe barbadensis miller_, is the most common species of Aloe that is cultivated for agricultural and medical purposes. It is a perennial succulent xerophyte with elongated leaves that contain a clear gel. While aloe vera has a long history of commercial uses, it is still widely used in cosmetic, food and pharmaceutical products. The use of aloe vera in constipation, inflammatory disorders, cancer, ulcer, and diabetes has also been investigated [A32476]. The active constituents of aloe vera include polysaccharides with protective effects on skin, as they exhibit antioxidant and anti-inflammatory properties [A32481]. Common active polysaccharides include glucomannans, polymannose, and acemannan, or b-(1–4)-acetylated polymannose [A32475]. Acemannan and other modified polysaccharides are responsible in preventing suppression of contact hypersensitivity or immune suppression induced by external factors such as irradiation [A32473].
Indication
Indicated for use as a topical agent to soothe sensitive skin and to relieve symptoms of various skin conditions, including contact or atopic dermatitis, eczema, dermatitis and acne urticata, first- and second-degree burns, radiation dermatitis, and sunburn.
Mechanism of Action
It is suggested that aloe polysaccharides mediate skin-protectant effects in damaged skin, induced by internal or other external factors such as radiation, via inhibiting apoptosis of normal cell lines _in vitro_ and thrombocytes _in vivo_ [A32473]. Following irradiation, aloe polysaccharides block the upregulation of pro-apoptotic p53, Bax, and Bad while blocking downregulating anti-apoptotic Bcl-2 [A32473]. _In vivo_, aloe polysaccharides may act as a scavenger for oxygen free radicals including DPPH, alkyl radicals, superoxides, and singlet oxygen and hydroxyl radicals that may also be generated by superoxides [A32470, A32476]. Hydrogen peroxide, which is a weak initiate lipid peroxidation, may also be effectively scavenged by aloe polysaccharides [A32476]. In a Fenton reaction system, aloe polysaccharides demonstrated a concentration-dependent scavenging activity against hydroxyl radical that were generated during the reaction [A32476]. Aloe polysaccharides may also compete with oxygen to react with nitric oxide (NO), thereby inhibiting the generation of nitrite and peroxynitrite anions that act as free radicals [A32476]. Findings from a study investigating the effects of aloe polysaccharides on doxorubicin-induced oxidative stress suggest that aloe polysaccharides mediate potent antioxidant actions _in vivo_ [A32476]. Doxorubicin, known to generate reactive oxygen species such as superoxide and hydroxy radicals, was administered to albino rats. This led to myocardial oxidative stress and cardiac injury accompanied by leakage of LDH and CPK from cardiac myocytes and to serum due to lipid peroxidation of cardiac membranes, reduced levels of antioxidant coenzyme GSH, and increased levels of SOD from a compensatory and combative mechanism of oxidative stress [A32476]. Treatment with aloe polysaccharides resulted in a significant decrease in serum LDH and CPK levels, indicating that aloe polysaccharides are capable in stabilizing cardiac membranes from peroxidative damage. Restored levels of endogenous GSH and SOD in a dose-dependent manner were also observed with the treatment of aloe polysaccharides, suggesting that aloe polysaccharides exhibit potent antioxidant properties [A32476]. In a study of rats with open cutaneous back wounds, treatment with aloe polysaccharides decreased the levels of matrix metalloproteinase-3 (MMP-3) and induced tissue inhibitors of matrix metalloproteinase-2 (TIMP-2) during the early stage of wound repair, resulting in decreased collagen breakdown and increased preservation of collagen content in the injured area [A32471]. A study proposes that acemannan, a common aloe polysaccharide, stimulates BMSC proliferation, ALPase activity, expression of VEGF, BMP-2, OPN, BSP, and mineralization leading to osteoblast differentiation and bone formation during socket healing [A32475].
Pharmacokinetics
- Absorption
- No pharmacokinetic data available.
- Distribution
- No pharmacokinetic data available.
- Metabolism
- No pharmacokinetic data available.
- Elimination
Clearance
No pharmacokinetic data available.
Toxicity
The oral LD50 value of aloe polysaccharides in a mouse toxicity study was 6.1 g/kg [A32476]. No cases of overdose reported.
Active Ingredient/Synonyms
Aloe vera leaf | Aloe Polysaccharide |
Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.
Description
Rhubarb allergenic extract is used in allergenic testing.
Active Ingredient/Synonyms
Rhubarb | Rhubarb |
Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.
Description
Sennosides (also known as senna glycoside or senna) is a medication used to treat constipation and empty the large intestine before surgery. The medication is taken by mouth or via the rectum. It typically begins working in minutes when given by rectum and within twelve hours when given by mouth. It is a weaker laxative than bisacodyl or castor oil. Sennoside A, one of the sennosides present in the laxative medication, has recently proven effective in inhibiting the ribonuclease H (RNase H) activity of human immunodeficiency virus (HIV) reverse transcriptase [A19231].
Indication
For the over the counter treatment of constipation [FDA Label].
Mechanism of Action
Sennoside A and B, the components of senna, are metabolized by gut bacteria into the active metabolite rheinanthrone [DB13175]. Rheinanthrone [DB13175] appears to increase cyclooxegenase 2 (COX2) expression in macrophage cells leading to an increase in prostaglandin E2 (PGE2) [A19235]. This increase in PGE2 is associated with a decrease in aquaporin 3 expression in mucosal epithelial cells of the large intestine. A decrease in aquaporin 3 expression likely produces the laxative effect by restricting water reabsorption by the large intestine thereby increasing fecal water content. The exact mechanism by which rheinanthrone increases COX2 expression is unknown. Rheinanthrone [DB13175] also stimulates peristalsis in he large intestine although the mechanism behind this effect is unknown [A19239]. Rhein [DB13174], another active metabolite is thought to excite submucosal acetylcholinergic neurons resulting in increased chloride and prostaglandin secretion. The movement of chloride ions into the large intestine would also help to draw water into the lumen [A19258].
Pharmacokinetics
- Absorption
- Distribution
- Metabolism
- Sennosides A and B are metabolised to sennidins A and B by gut bacteria [A19239]. Sennidins A and B are further metabolized to rheinanthrone [DB13175] by gut bacteria using beta-glucosidase [A19235]. Rheinanthrone [DB13175] is absorbed into systemic circulation where 2.6% is metabolized to rhein [DB13174] and sennidins A and B via oxidation [A19237] [A19248] [A19235]. Rheinanthrone [DB13175] is the major active metabolite of sennosides A and B which produces the laxative effect of the medication. Rhein [DB13174] is also an active metabolite known to have many protective effects [A19247].
- Elimination
Toxicity
Senna causes increased amounts of apoptosis in the large intestine shortly after use due to upregulated p53 activity [A19236]. This is normally reversed after 18 hours however chronic use has been shown to be associated with p53 resistance and potential carcinogenicity leading to colon cancer. The LD50 value in rats was 5000mg/kg. Subacute studies in rats receiving 20mg/kg and dogs receiving 500mg/kg did not produce signs of toxicity [A19238]. Tests for mutagenicity and reproductive toxicity do not indicate toxic effects.
Active Ingredient/Synonyms
Senna | Senna glycosides | Sennoside | Sennosides | Sennosides |
Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.