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metformin hydrochloride (Riomet ER)

✓ Approved

Sun Pharmaceutical Industries Ltd. · Small Molecule · Small Molecule

What is metformin hydrochloride?

metformin hydrochloride is a small molecule developed by Sun Pharmaceutical Industries Ltd.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesRiomet ER
CompanySun Pharmaceutical Industries Ltd.
Drug ClassSmall Molecule
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Sun Pharmaceutical Industries Ltd.

Therapeutic Indications

metformin hydrochloride is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Metabolism and nutrition disordersType 2 diabetes mellitus✓ Approved

Related Research Articles

PubMedFuture science OA2026-11-11

Distinct associations of STK11 rs2301759 and SLC29A4 rs2685753 with metformin response among Saudi patients with type 2 diabetes mellitus.

Althomali Abdullah A, Issa Noha M NM, Al-Asiri Ibrahim S IS, Algarni Misfer S MS et al.

This study investigates the genotype and allele frequencies of solute carrier family 29 member 4 (SLC29A4) rs2685753 and serine/threonine kinase 11 (STK11) rs2301759 in the Saudi population and their association with metformin response in Saudi patients with type 2 diabetes mellitus (T2DM), while comparing the findings with other ethnic populations. A prospective cohort study included 69 newly diagnosed Saudi adults with T2DM receiving metformin monotherapy for at least six months and 59 healthy controls. Genotyping was performed using TaqMan single-nucleotide polymorphism (SNP) assays. Associations between genetic variants and glycemic response were analyzed using chi-square tests and logistic regression. Among patients, 55% achieved adequate glycemic control, whereas 45% were non-responders. SLC29A4 rs2685753 showed no significant association with the metformin response. In contrast, STK11 rs2301759 demonstrated significant genotypic and allelic associations, with the C/T genotype linked to improved glycemic response. Higher baseline glycated hemoglobin (HbA1c) and family history of diabetes were associated with poorer response. STK11 rs2301759 may influence metformin efficacy in Saudi patients with T2DM and could support personalized diabetes management.

PMID 43010183
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PubMedMedicine2026-11-11

Effectiveness of metformin as initial treatment on the metabolic profile of Saudi patients newly diagnosed with type 2 diabetes mellitus: A prospective observational study.

Alkreathy Huda H, Alharbi Fawaz Abdullah FA, Magadmi Rania R, Hakami Alqassem Y AY et al.

The incidence of diabetes is increasing in several countries, including Saudi Arabia. Metformin is a common treatment for type 2 diabetes mellitus (T2DM); however, its effect on the metabolic profile of patients newly diagnosed with T2DM remains unclear. To evaluate the effects of metformin on the metabolic profile, including hemoglobin A1c (HbA1c) and lipid levels, in patients newly diagnosed with T2DM in Madinah, Saudi Arabia. This prospective observational study involved 82 participants newly diagnosed with T2DM. The participants were aged between 30 and 65 years, and their HbA1c level was ≥6.5% higher than the normal range. None of them had taken any oral hypoglycemic medication before metformin treatment. Fourteen patients did not undergo regular follow-ups. A total of 68 patients completed the study. The primary outcomes were changes in HbA1c, cholesterol, low-density lipoprotein (LDL), and hepatic enzyme marker levels. The HbA1c level significantly reduced after the 12-week treatment period (6.85% vs 7.29% at baseline, P = .001). Furthermore, 67.3% of the patients exhibited a noteworthy decrease in cholesterol (4.68 vs 5.18 mmol/L at baseline, P = .014) and LDL levels (3.03 vs 3.52 mmol/L at baseline, P = .006). However, no significant changes were observed in the levels of the other lipid profile markers. Various dosages of metformin showed comparable effects in reducing HbA1c, cholesterol, and LDL levels, but inconsistent effects on hepatic enzymes. The results suggest that metformin can be considered an initial treatment option for patients newly diagnosed with T2DM. These findings are significant given the increasing prevalence of diabetes in Saudi Arabia and the need for effective and safe treatment options. Further studies are required to explore the pharmacogenomics and metabolomics of metformin in this specific population.

PMID 43012773
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PubMedCell discovery2026-11-11

ER-mitochondria contacts orchestrate mitochondrial transport via C19orf12.

Pei Xiayuhe X, Zhang Shuqian S, Li Peiyang P, Wu Yutong Y et al.

Endoplasmic reticulum (ER)-mitochondria contact sites facilitate lipid transfer, calcium signaling, and mitochondrial division; however, their role in mitochondrial transport remains unclear. Here, we identify hereditary spastic paraplegia (HSP)-associated protein C19orf12 as an ER-anchored regulator of mitochondrial trafficking. The loss of C19orf12 leads to perinuclear mitochondrial clustering in cells, impaired anterograde transport in neurons, and progressive locomotor dysfunction in mice that recapitulates key features of HSP in humans. Mechanistically, C19orf12 forms a discrete complex with the mitochondrial Rho GTPase Miro1 and the Kinesin-1 motor Kif5b, thereby providing a molecular link between ER-mitochondria contacts and microtubule-based anterograde transport. Ca2+ also modulated C19orf12-Miro1 behavior in vitro and showed a biphasic association with mitochondrial motility in live cells. Therefore, our findings establish ER‒mitochondria contact sites as logistical hubs for Kinesin-1 motor loading and highlight the importance of the Ca2+-tunable C19orf12 scaffold in sustaining directional mitochondrial transport, providing a mechanistic framework for how C19orf12 loss may contribute to neurodegeneration.

PMID 43009488
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PubMedAdvanced healthcare materials2026-11-11

Sequential Modeling of Fibrotic and Mineralizing Osteoarthritis-Like Remodeling in hDPSC-Derived Cartilage Microtissues.

Huang Xinqi X, Tao Yun Y, Huang Zhimao Z, Zhao Zhihe Z et al.

Osteoarthritis (OA) involves alterations in cartilage mechanics, matrix composition, and mineralization, yet in vitro models that resolve remodeling transitions remain limited. Scaffold-free cartilage microtissues derived from human dental pulp stem cells (hDPSCs) are subjected to sequential dynamic rocking culture and triiodothyronine (T3) treatment. Dynamic rocking produces superficial Col I-positive fibrotic and matrix-degrading changes, whereas T3 induces proteoglycan loss, increased Col I and MMP13, irregular mineral deposition, and altered nanomechanical properties, defining a mixed terminal catabolic and mineralizing OA-like state. Transcriptomic profiling shows stage-associated reorganization rather than uniform pathway activation. In T3-treated microtissues, ATF6-associated ER-stress abnormalities include ER cisternal dilation and increased ATF6 signal. Targeted ATF6 knockdown reduces ATF6 signal, ER dilation, extracellular-matrix disorganization, and ER-stress/proteostasis and inflammatory/catabolic transcriptional module scores, supporting ATF6-associated signaling as a functionally relevant component of this degenerative state. In mouse temporomandibular joint and knee OA models, intra-articular Ad-shATF6 is associated with partial cartilage preservation and subchondral-bone indices shifted toward control ranges.

PMID 43012460
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PubMedThe Biochemical journal2026-11-11

Ribosomal RNA depurination prevents the unfolded protein response through translation inhibition.

Prashar Tanya T, Hudak Katalin A KA

Many newly translated proteins are targeted to the endoplasmic reticulum (ER) for folding, processing and transport to extracellular spaces. The unfolded protein response (UPR), mediated by the ER stress sensor Ire1 that splices mRNA of transcription factor Hac1, is activated when unfolded proteins accumulate. However, it remains unclear how ribosome integrity, through its effects on translation, controls UPR. To address this question, we expressed pokeweed antiviral protein (PAP), an rRNA N-glycosylase that depurinates 25S rRNA in Saccharomyces cerevisiae. We compared the effect of PAP with an enzymatically inactive mutant PAPx, as both proteins are targeted to the ER during translation, but only one damages ribosomes. RNA sequencing across a six-hour time course revealed enrichment of the ER protein processing pathway and selective upregulation of UPR-related genes in PAPx-expressing cells, but not in PAP-expressing cells. PAPx expression also increased HAC1 splicing, whereas PAP did not, even after tunicamycin treatment. Additionally, Ire1 remained inactive, as shown by lack of Ire1-2xGFP oligomerization viewed by confocal microscopy. Absence of UPR activation in PAP-expressing cells was correlated with reduced azidohomoalanine (methionine analog) incorporation into membrane-associated proteins, consistent with reduced protein flux into the ER. Our findings support a new model describing how rRNA depurination inhibits UPR upstream of Ire1 activation by reducing translational capacity, which maintains Ire1 in an inactive state. Therefore, ribosome integrity influences UPR activation by controlling translation and membrane-associated protein synthesis.

PMID 43012403
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PubMedNano letters2026-11-11

ROS-Responsive Selenocysteine-Releasing Nanozyme for Targeted Ferroptosis Suppression and Pancreatic β-Cell Protection in Type 2 Diabetes.

Zhang Juncai J, Li Yuqi Y, Xie Yingying Y, Wang Runqi R et al.

Pancreatic β-cell ferroptosis, driven by oxidative stress and impaired glutathione peroxidase 4 (GPX4) activity, has emerged as an important contributor to the progression of type 2 diabetes mellitus (T2DM). However, persistent reactive oxygen species (ROS) accumulation and insufficient selenocysteine (Sec) availability limit GPX4-dependent antioxidant defense, making effective ferroptosis intervention challenging. Here, we engineered a ROS-responsive Sec-loaded copper-based single-atom nanozyme (Se@CuSAzyme) that combines catalytic ROS scavenging with Sec supplementation. Benefiting from its intrinsic superoxide dismutase- and catalase-like activities, Se@CuSAzyme efficiently eliminated excessive ROS, while oxidative stress-triggered Sec release enhanced GPX4 expression. As a result, Se@CuSAzyme markedly suppressed high glucose and erastin-induced ferroptosis, reduced lipid peroxidation, and preserved mitochondrial integrity in pancreatic β-cells. In high-fat diet/streptozotocin-induced diabetic mice, Se@CuSAzyme demonstrated therapeutic efficacy comparable to that of metformin in ameliorating hyperglycemia, alleviating insulin resistance, and increasing energy expenditure. Importantly, Se@CuSAzyme outperformed metformin in protecting against hepatic steatosis and glycolipid metabolic dysfunction.

PMID 43012594
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