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POM TR. 033 318 421
(Distribution Permit Number from Board of Drug and Food Control the Republic of Indonesia)


 is a freeze dried Ganoderma lucidum Polysaccharide Peptide (GLPP) extract from mycelium cell wall. Each capsule contains 250 mg of Polysaccharide Peptide, which it equal to 180 mg β-1,3/1,6-D-Glucan.

β-1,3/1,6-D-Glucan is an immunomodulator that modulates immune cell activities, especially macrophages. β-1,3/1,6-D-Glucan works on several human immune receptors such as Dectin-1 (the main receptor), Toll-like Receptor 2 and 6 (TLR-2 and -6), Scavenger Receptor, Complement Receptor 3 (CR3), and Lactosylceramide. It induces a group of immune cells such as macrophages, neutrophils, monocytes, Natural Killer (NK) cells and dendritic cells to modulate the innate and adaptive immune responses. β-1,3/1,6-D-Glucan is absorbed by M cells in the intestine and then phagocytized and degraded by macrophages in the Peyer’s patches. Macrophages that contain β-1,3/1,6-D-Glucan will circulate in the spleen and lymph nodes and release smaller fractions of β-1,3/1,6-D-Glucan particles to activate other immune cells. In bone marrow these macrophages will also release β-1,3/1,6-D-Glucan particles to activate bone marrow stem cells.(1,2)

* for detailed information, please see product application


  • Extract of Ganoderma lucidum Polysaccharide Peptide (GLPP) 250mg
  • Containing β-1,3/1,6-D-Glucan 180mg
  • Filler up to 100mg


To modulate the immune system (immunomodulator) and to be used as a complementary therapy against cancer, cardiovascular diseases, vascular endothelial disturbances, infectious diseases, and inflammatory bowel diseases.


  • Hypersensitivity to the ingredients of the mushroom and other ingredients used in this product


  • Stop using when undesirable symptoms occurred. Please consult your doctor

Adverse Reaction

  • Sub febrile and allergic reaction is rare, but can occur in few people (individually)


  • 3x1 capsules / day


  • ½ hour before or 1 hour after meals


  • Keep in dry and cool place


Box of bottle with security seal protection @ 30 capsules 

Description : Each capsule contains 250 mg of polysaccharide peptide extract from Ganoderma lucidum mycelium

Active Constituent Analysis

SLH Product’s Specification/



(Consist of glucose, mannose, xylose, fucose, galactose and linked by b-glycosidic linkages)                                                  

min. 250 mg

Phenol Sulfuric Acid

β–1.3/1.6-D-Glucan content in Polysaccharides

min. 180 mg

Congo Red


min. 10 mg


Heavy Metal



≤ 0.5 ppm



≤ 0.3 ppm


≤ 10 ppm


≤ 5 ppm

Typical Microbiological Analysis


Total bacterial count

< 30 cfu/g

USP Method 61

Total yeast and mould count

< 30 cfu/g

Salmonella Sp.


Indonesian Pharmacopeia 4th Ed. 1995

Escherichia coli


Staphylococcus aureus


Pseudomonas aeruginosa


Shigella Sp.


Culture & Identification

Physical Properties




Organoleptic Test


Yellow brown


Typical mushroom



Moisture Content

≤ 10 %

Indonesian Pharmacopeia 4th Ed. 1995




1 bottle @ 30 capsules


Keep in dry and cool place, avoid direct sun contact

Document Number : SLH/SPESI/QC/04/001
The information contained herein is believed to be true and reliable.

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A.  as Complementary Therapy in Cancer

Cancer is a dangerous disease which is characterized by an abnormal and uncontrolled cell growth that is able to spread (metastasize) to many organs. Due to its characteristics, cancer often results in death. Another term for cancer is “malignant tumor”. There are two types of tumor: benign (non-cancerous tumors) and malignant (cancerous tumors). The differences between both types are the ability to spread to many organs. A malignant tumor is able to invade and metastasize to other organs.(1)

Until now conventional therapies against cancer, such as surgery, chemotherapy and radiotherapy, still reach low success rates in a large number of cancer types. At present the use of complementary therapy from isolated natural products is starting to receive gaining interest in cancer treatment. A well known natural product that is used as complementary therapy against cancer is Ganoderma lucidum (GL) with β-D-Glucan as its bioactive substance.

is a Ganoderma lucidum polysaccharide peptide (GLPP) extract from mycelia. Each capsule contains 250 mg of polysaccharide peptide, in which it has 200 mg β-D-Glucan (180 mg β-1,3/1,6-D-Glucan). β-D-Glucan is an immunomodulator that modulates immune cells activities, especially macrophages.

β-D-Glucan works on several human immune receptors such as Dectin-1 (the main receptor), Toll-like Receptor 2 and 6 (TLR-2 and -6), Scavenger Receptor, Complement Receptor 3 (CR3), and Lactosylceramide. It induces a group of immune cells such as macrophages, neutrophils, monocytes, Natural Killer (NK) cells and dendritic cells to modulate the innate and adaptive immune responses. β-D-Glucan is then absorbed by colon peyer patch, and later on phagocyted and degraded by macrophages. Macrophages that contain β-D-Glucan will circulate in the spleen and lymph nodes and release smaller fractions of β-D-Glucan particles to activate other immune cells via the binding of β-D-Glucan with CR-3. These immune cells later are recruited to tumor cell which are coated with antibody and destroy it. In bone marrow these macrophages will also release β-D-Glucan particles to activate bone marrow stem cells.(2-4)

Fig. 5. Mechanism of Action of β-D-Glucan (PsP) as an Immunomodulator

B.  as Chemoradioprotector in Cancer Therapy

Chemotherapy is a standard therapy in cancer. Unfortunately, chemotherapy eliminates not only cancer cells but also normal cells especially ones that proliferate quickly, such as gastrointestinal tract epithelial, hair follicle, nail and skin cells. There are several reasons that make chemotherapy ineffective. Chemotherapy is often followed by immunosuppression and neutropenia, which trigger infection and metastasis, and multidrug resistance (MDR) phenomenon. MDR appears due to the high increase in the level of P-glycoprotein (P-gp) or multidrug resistance-associated protein (MRP), causing chemotherapy agents to pump out of cancer cells.(5) Until now, chemotherapy only reaches low efficacy rates, such as in leukemia and lung cancer.

In vitro study shows that GLPP inhibits leukemic cancer cell resistance to adriamycin (K562/ADM) and human small cell lung cancer (SCLC) resistance to etoposide and doxorubicin.(5,6)

Fig. 6. GLPP inhibits Multidrug Resistance in Cancer Treatment

Ganoderma lucidum Polysaccharide Peptide (GLPP) which contains β-D-Glucan inhibits hematotoxicity due to chemotherapy-induced myelosuppression, which presents as neutropenia, leucopenia and thrombocytopenia. A phase I/II clinical study of β-D-Glucan in the treatment of patients with advanced malignancies receiving chemotherapy showed that β-D-Glucan was able to improved hematopoiesis and reduce leucopenia and thrombocytopenia.(7,8)

Fig. 7. GLPP promotes Myelopoiesis

Another standard therapy in cancer is radiotherapy which uses x or γ-rays to destroy cancer cells. Unfortunately, radiotherapy also decreases thymus, spleen’s weight and lymphocyte counts. Radiation also affects bone marrow around radiated-organs and causes myelosuppression. In a in vivo study it was shown that GLPP was able to increase thymus weight and splenocyte proliferation of γ-irradiated mice.(9)

Due to the above mentioned beneficial effects of β-D-Glucan,  is used as chemoradioprotector for cancer patients who receive chemo and/or radiotherapy.

C.  as Complementary Therapy in Myocardial Ischemia

Myocardial ischemia occurs if oxygen and nutrients supply for cardiomyocytes supplied by coronary arteries is imbalanced with the cardiomyocyte demand. This imbalance is mainly caused by atherosclerotic plaque in the coronary artery circulation. Myocardial ischemia is also associated with inflammation and a cytokines cascade resulting in myocardial infarction and the subsequent development of heart failure (HF).(10)

Coronary Artery Bypass Grafting (CABG) is a standard surgical procedure to restore the blood flow into the heart. Two crucial points that comes to our attention about this process would be that there is a possibility that this procedure could be followed by inflammation and that there is a decrease in cardiomyocytes conractile capability, which is identified as “low cardiac output syndrome”, that affects 9% of the patiens who under go CABG.(11)

In ischemia or reperfusion conditions, cytokines activate the Nuclear Factor-kB (NF-kB) signaling pathway through Toll-like Receptor-4 (TLR-4) on the cardiomyocytes surface. As a result cardiomyocytes apoptosis occurs. β-D-Glucan with its cardioprotective effect on ischemia-reperfusion injury is able to bind with TLR-4 and shift the NF-kB signaling pathway towards the Phosphoinositide3-kinase (PI3K) signaling pathway resulting in cardiomyocytes survival. In a clinical study it was proved that pretreatment with oral β-D-Glucan for patient undergoing CABG resulted in cardioprotective effects as demonstrated by myocardial enzyme depletion in blood. (11,12)

In 2013, , in collaboration with Faculty of Medicine Brawijaya University (Malang- East Java, Indonesia), conducted a pre-clinical study of  in in vivo model of atherosclerosis and type II Diabetes Mellitus. The result of this study demonstrates the ability of  in inhibiting atherosclerosis progressivity through its mechanism of action as anti-inflammation and anti-oxidant. The anti-inflammatory activity of  is confirmed by the reduction of Interleukin-6 (IL-6) and high sensitive-C Reactive Protein (hs-CRP) level in blood; whereas the anti-oxidant activity of PsP is confirmed by the reduction of Malondealdehyde (MDA) as end product of lipid peroxidation which causes oxidative stress to vascular cells. The anti-oxidant activity of PsP is also able to increase the level of antioxidant enzyme Superoxide Dismutase (SOD) in blood. The improvement of lipid profile is in the form of the reduction of Total Cholesterol (TC) and Low-density Lipoprotein (LDL), which also describes the enhancement of High-density Lipopropotein (HDL) in PsP treatment group. The reduction of foam cell formation in  treatment group also supports the proof that PsP can be used to inhibit progressivity of atherosclerosis.(13,14). A detailed explanation about PsP’s preclinical study can be reviewed for your perusal at

In a study it was observed that macrophages in Peyer’s patch would phagocytized orally administrated β-D-Glucan to smaller fragments. These β-D-Glucan fragments were then transported and released in bone marrow where they could bind with Complement Receptor 3 (CR3) in the bone marrow stem cells. This binding stimulated complement activation that caused stem cells to proliferate, differentiate and recruit into injury site which expressed iC3b including injured cardiomyocytes.(15) β-D-Glucan in  would bind with CR3 in bone marrow and cardiac stem cells, stimulate complement system activation and induce stem cells to proliferate, differentiate and recruit into injured cardiomyocytes to replaced them.

Fig. 9. β-D-Glucan Stimulates Stem Cell Proliferation, Differentiation and Recruitment to the Site of Injury 

D.  as a Complementary Therapy in Hepatitis B and C, Fibrosis and Cirrhosis

Viral Hepatitis B and C (HBV and HCV) generally proceeds to chronic hepatitis, fibrosis, cirrhosis and even liver cancer (hepatocellular carcinoma/HCC). In recent findings, the standard therapies for viral hepatitis infection are Interferon-α (IFN-α) and nucleoside analog (anti-viral), although the efficacy of both therapies are low. In addition, the long term use of analog nucleoside can exert resistance because the HBV and HCV are known to have high mutation rate.

The immune system plays an important role in HBV or HCV elimination which is mediated by cytotoxic T lymphocyte (CTL). The binding of β-D-Glucan with its receptor in immune cells, mainly in macrophages, results in cascade activation of cytokine secretion in other immune cells including CTL response to HBV and HCV.

In a clinical study it was shown that chronic hepatitis B patients who received GLPP for 3 months resulted in HBV DNA and HBeAg depletion in 25% patients. 6 months follow up resulted in HBsAg negative in 13% patients. This percentage was high (significant difference) compared to the group of control patients (not receiving GLPP). As an immunomodulator, Ganoderma lucidum antiviral activity works through the inhibition of: (16,17)

  • viral hepatitis absorption and fusion with hepatocytes
  • viral hepatitis endocytosis, integration and assembly in hepatocytes
  • viral hepatitis release from hepatocytes

Viral hepatitis is not the only factor that causes chronic hepatitis. Other factors are alcohol, drug abuse, and also metabolic disease. Chronic hepatitis usually develops into abnormal accumulation of extracellular matrix (ECM) in the liver and becomes cirrhotic with poor prognosis result in HCC.

GLPP’s hepatoprotective properties are antioxidative and antifibrotic. As an antioxidant GLPP prevents hepatocytes damage through its free radical scavenger mechanism. With its antifibrotic activity GLPP inhibits hydroxyprolline synthesis (ECM component) through hepatic stellate cells (HSC) activated by proinflammation cytokine (TNF-α and IL-1β) in chronic inflammation. Due to the above properties,  is used as complementary therapy in chronic hepatitis B and C, fibrosis, cirrhosis and HCC.(18)

E.  as Complementary Therapy in Diabetic Foot Ulcer

Diabetic foot ulcer is a diabetic complication that is hard to overcome. Hyperglycemia causes endothelial abnormalities (microcirculation deficiency), neuropathy and wound cells (macrophages and fibroblasts) abnormalities resulting in wound healing delay.(19)

Depletion of endothelial Nitric Oxide Synthetase-derived Nitric Oxide (eNOS-derived NO) as a vasodilator, basement membrane thickening and reduction of capillary size are caused by microcirculatory deficiency. As a result leucocytes cannot reach wound area for inflammation process to clean the debris and prevent infection. (19)

Diabetic neuropathy usually affects sensory, motoric and autonomic nerves. This neuropathy causes the patient to be unaware of their initial wound until the wound becomes a severe ulcer.(19)

Macrophages and fibroblasts are very vital in the wound healing process. Diabetic hyperglycemia inhibits macrophages from secreting cytokines, such as Tumor Necrosis Factor-α (TNF-α), Interleukin-1β (IL-1β) and growth factors: Vascular Endothelial Growth Factor (VEGF), Platelet Derived Growth Factor (PDGF), basic Fibroblast Growth Factor (bFGF). These cytokines are necessary to activate angiogenesis and lymphangiogenesis during wound healing process. Synthesis of collagen by fibroblasts to increase tensile strength is impaired due to the hyperglycemia condition. (20)

Under the influence of the immune system wound healing processes are heavily depended on macrophages, fibroblasts, keratinocytes with cytokines, and growth factors. As a consequence agents or substances with immunomodulatory activity play a significant role in the reparative process. (21)

β-D-Glucan in  is able to induce macrophages to secrete growth factor (VEGF) which is needed for angiogenesis and lymphangiogenesis in the wound healing process. β-D-Glucan is also able to stimulate fibroblasts to synthesize collagen. Systemic or oral β-D-Glucan administration enhances the wound healing process itself and stimulates macrophages infiltration to wound area, tissue granulation, collagen deposition, re-epithelization and tensile strength. Due to the properties of β-D-Glucanmentioned above,  should be used as complementary therapy in diabetic foot ulcer.(22-24)

Fig. 10. The Effects of β-D-Glucan on Macrophage and Fibroblast in the Wound Healing Process

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The clinical trial for cardiovascular diseases was conducted at the Department of Cardiology, Dr. Saiful Anwar General Hospital-Brawijaya University, School of Medicine, Malang, East Java, Indonesia in 2015 with Prof. H. Djanggan Sargowo, MD., Ph.D., FACC, FESC, FAPSC as Chief Investigator.


This clinical trial is using a true experimental study research method with pre-test and post-test design that recruited:

  • 35 Stable Angina Pectoris subjects
  • 37 High-risk heart disease subjects, according to Framingham Risk Score > 20


Average age of the subjects was 65 years.


Dosage  :  3×1 capsule/day
Duration  : 90 days*

*as an adjuvant therapy to the standard therapy that was regularly administered by subjects in accordance to their needs.


The biomarkers measured during the pretest and post test:

  1. Inflammation: Interleukin-6 (IL-6), Tumor Necrosis Factor-α (TNF-α), and C-Reactive Protein (CRP)
  2. Oxidative Stress: Malondialdehyde (MDA) and Superoxide Dismutase (SOD)
  3. Lipid Profile: Total Cholesterol (TC), Triglycerides (TG), Low-density Lipoprotein (LDL) and High-density Lipoprotein (HDL)
  4. Endothelial Dysfunction: Circulating Endothelial Cell (CEC) and Endothelial  Progenitor Cell (EPC)
  5. Diabetes: Glycated Hemoglobin (HbA1c).

Clinical Trial Results

Effect of PsP Administration on Inflammatory Biomarkers, i.e. IL-6, TNF-α and CRP

Atherosclerosis in Angina Pectoris involves a chronic inflammatory process that occurs at every stage of atherosclerosis. Therefore, measurements of TNF-α, CRP, and IL-6 levels as inflammatory biomarker were performed to determine the effect of PsP on the inflammatory process.

Figure 1. Effect of PsP Administration on IL-6 Levels in Groups of Patients with Stable Angina Pectoris and High-Risk Cardiovascular Disease

Figure 2. Effect of PsP Administration on TNF-α and CRP Levels in Groups of Patients with Stable Angina Pectoris and High-Risk Cardiovascular Disease

Biomarker measurements after 90 days of the use of PsP as an adjuvant therapy to the standard therapy demonstrated a significant decrease of IL-6, TNF-α, and CRP levels. Thus, PsP does act as an anti-inflammatory agent in suppressing atherosclerosis progress.

Effect of PsP Administration on Oxidative Stress, i.e. MDA, SODs and NO

Parameters of oxidative stress measurement are MDA, SODs and NO. MDA and NO are biomarkers that indicate the presence of lipid peroxidation by Reactive Oxygen Species (ROS), while SODs performs in suppressing oxidative stress by catalyzing the reaction of superoxide anion (O2–) dismutation into hydrogen peroxide.

Figure 3. Effect of PsP Administration on MDA, SODs and NO Levels in Groups of Patients with Stable Angina Pectoris and High-Risk Cardiovascular Disease

Biomarker measurements after 90 days of the use of PsP as an adjuvant therapy to the standard therapy showed adjustments on the following values:

  • a decrease in the MDA level
  • an increase in the SODs level
  • a decrease in the NO level compared to prior to PsP administration.

This data suggests that oxidative stress is suppressed by PsP administration.

Effect of PsP Administration on Lipid Profiles, i.e. TC, LDL, TG and HDL

In this clinical trial the lipid biomarkers were measured to discover about the condition of dyslipidemia, which has an important role in the increase of heart disease risk through high levels of LDL and TG, and low HDL levels.

Figure 4. Effect of PsP Administration on Total Cholesterol and LDL Levels in Groups of Patients with Stable Angina Pectoris and High-Risk Cardiovascular Disease

Figure 5. Effect of PsP Administration on TG and HDL Levels in Groups of Patients with Stable Angina Pectoris and High-Risk Cardiovascular Disease

Biomarker measurement after 90 days of the use of PsP as an adjuvant therapy to the standard therapy showed adjustments on the following values:

  • a decrease in Total cholesterol, LDL and TG levels
  • no increase in HDL level

Thus, PsP may help improve the condition of dyslipidemia.

Effect of PsP Administration on the Endothelial Dysfunction Biomarkers, i.e., CECs and EPCs

Endothelial dysfunction biomarkers measured during this clinical trial were:

  • Circulating Endothelial Cells (CECs)
  • Endothelial Progenitor Cells (EPCs)

The CEC counts in patients with acute coronary syndromes correlate with endothelial dysfunction and with the prothrombotic state, hence, CECs can act as a blood-based biomarker of cardiovascular diseases. CECs are considered to reflect the occurrence of endothelial defects and vascular disruption, and serve as a biomarker that answers to both diagnostic and prognostic needs. CECs are rarely found in normal healthy individuals, in the order of < 3 cells/ml.

In parallel is the hypothesis that EPCs are restorative/regenerative cells, possible destined to replace/renew damaged areas of the intima.

Thus it can be concluded that CECs is a biomarker of vascular damage. High levels of CECs indicate endothelial damage whereas EPCs is a vascular repair biomarker.

Figure 6. Effect of PsP administration on CECs and EPCs levels in Groups of Patients with Stable Angina Pectoris and High-Risk Cardiovascular Disease CECs

The significant reduction of CEC in this study, for both high risk and stable angina patients suggest the improvement of endothelial dysfunction in atherosclerosis after PsP administration.

The decreased numbers of CECs indicate an improvement in endothelial cells; therefore, in cases of increase of CECs numbers such as in cardiovascular disease and its risk factors, i.e. unstable angina, acute myocardial infarction, stroke, diabetes mellitus, critical limb ischemia, a decrease in the number of CECs is expected to happen.

This study results show a significant reduce of CEC and EPC. As the CEC is reduced, so there is minimal detachment of endothel and injury in endothelial cells, suggesting that the endothelial cells do not need high turnover rate to maintain vessel homeostasis, and will not induce the mobilization of EPC. In myocardial infarction, EPC markedly increased with peak values on day 7, and returned to baseline within 60 days.

Since this study was only 90 days, the significant reduction of EPC remains a debate whether because of the minimal endothelial injury that was not enough to induce EPC mobilization, or decreasing EPC mobilization due to effect of β-glucan. Whereas, the research of Hristov M. et al., states that within 3 – 4 weeks EPCs have formed monolayers with endothelial appearance.

Thus, PsP administration does improve endothelial function by its antioxidant effects.

Effect of PsP Administration on Diabetes Mellitus HbA1C Biomarker Profile

In this clinical trial one of the biomarker profiles of Diabetes Mellitus, Glycated (Glycosylated) Hemoglobin, known as HbA1c, was also measured. The HbA1c represents blood glucose levels that react with the 120 day old hemoglobin of red blood cells. Increased levels of glycated hemoglobin has been associated with cardiovascular disease, nephropathy, and retinopathy in diabetes mellitus.

Figure 7. Effect of PsP administration on Diabetes Mellitus HbA1C biomarker profile in Group of Patients with Stable Angina Pectoris and High-Risk Cardiovascular Disease

Biomarker measurements after 90 days of PsP administration to the standard therapy showed that:
PsP was able to decrease the HbA1c level in both groups of study subjects, i.e. groups of patients with Stable Angina Pectoris and High Risk Heart Diseases.

Decreased number of CECs and decreased in HbA1c levels prove that PsP may be administered by Diabetes Mellitus patients to prevent further vascular complications.


This clinical trial concludes that:
PsP can be used as secondary preventive therapy for patients with Stable Angina Pectoris and as primary preventative therapy for patients with High Risk Heart Disease (according to the Framingham Risk Score > 20).